Medical Immunology

Section 1 Introduction
 Definition of immunity
In the traditional sence ： In medical terms, immunity means protection from certain diseases, particularly infectious
diseases.
In the modern sence：Immunity means the physiological ability of immune system to discriminate between “self” and
“nonself” by inducing the tolerance to self-antigens and the elimination of foreign antigens.

Chapter 1 General Introduction

Components of immune system
Immune Organ Immune Cell Immune Molecule
central immune organ peripheral immune organ membrane secreted
bone marrow lymph node Innate immunity TCR Ab
thymus spleen Phagocyte BCR C
DC
MALT NK CD CK
NKT AM
…… MHC
adaptive immunity
T cell
B cell
…

Functions of immune system

Three functions: immune defense, immune surveillance and immune homeostasis.
Physiological Response Pathological Response
Immune Defense eliminate microbes and other foreign substances hypersensitivity,
immunodeficiency disease
Immune Surveillance eliminate transformed or aberrant cells tumor,
continuous virul infection
Immune Homeostasis immunological tolerance and immunological regulation autoimmune disease,
hypersensitivity disease
Immune response
 Classification innate immunity (non-specific immunity)
adaptive immunity (acquired immunity/specific immunity)
 Characteristics of innate immunity: inborn, immediate protection, no specificity, no memory.
 Characteristics of adaptive immunity: acquired, later protection, specificity, tolerance, memory.
Adaptive immunity
 cellular immunity (mediated by T cells）
 humoral immunity (mediated by B cells)

Chapter 2 Brief History of Immunology

Clonal selection theory
 Individual lymphocyte expresses membrane receptors that are specific for a distinct antigen, this unique
receptor specificity is determined before lymphocyte is exposed to the antigen;
 Lymphocytes with receptors against self are deleted from an early stage and are absent from the repertoire of
mature lymphocytes;

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 Binding of antigen to its specific receptor activates the cell, causing it to proliferate into a clone of cells that
have the same immunologic specificity as that of the parent cells.

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Section 2 Immune Organs and Tissues

Components and biological functions of immune organs
central immune organs ( primary lymphoid organs )
 bone marrow and thymus;
 where immune cells are generated and differentiate into mature cells.
peripheral immune organ ( secondary lymphoid organ )
 lymph nodes, spleen and MALT( mucosal-associated lymphoid tissue);
 where mature immune cells reside and most immune responses launched.

Chapter 1 Central Immune Organ

 Functions of bone marrow
 Hematopoiesis: the site of generation of all circulating blood cells in the adult, including immune cells;
 The site of B cells and NK cells maturation;
 One of the organs where the secondary humoral immunity happens.
 Functions of thymus
 The site of T cells maturation;
 Immunological regulation;
 Setup and maintenance of self tolerance.

Chapter 2 Peripheral Immune Organ

Functions of lymph nodes
 Where mature T lymphocytes and B lymphocytes reside;
 Where immune response to lymph-borne antigens launched;
 Participate lymphocyte recirculation;
 Filtration.
Functions of spleen
 Where mature T lymphocytes and B lymphocytes reside;
 Where immune response to blood-borne antigens launched;
 Synthesis of some biological substances;
 Filtration for the blood.
Mucosal-associated lymphoid tissue(MALT)
 Definition: MALT are diffuse lymphoid tissues which lie just below the mucosal epithelia in many regions of the
respiratory, alimentary and genitourinary tracts, including lymphoid tissues with germinal centers(tonsil, Peyer’s
patches and appendix), and they are the mainly sites where mucosal immune responses launched.
 Function: participate local mucosal immune response; produce secretory IgA(SIgA).

Chapter 3 Lymphocyte Homing and Recirculation

Definition of lymphocyte homing
After leaving central immune organ, mature lymphocytes migrate and reside in some definited region of
peripheral immune organ and tissue. This tissue-selective homing pattern results from interactions between
surface molecules on lymphocytes(homing receptor) and endothelial cells (vascular addressin).
Definition of lymphocyte recirculation
 Definition: lymphocytes recirculate between lymphatic system and blood system.

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Section 3 Antigen
Definition of antigen(Ag): Any substance capable of inducing an immune response is called an antigen, which usually
refers to substance that can be recognized by TCR or BCR, active T cells or B cells to proliferate, differentiate and to
generate specific lymphocytes and antibodies, and so can serve as the target of an immune response.

Charpter 1 Properties and Molecular Structure Base of Antigen

Properties of antigen
 Immunogenicity: The ability of antigen to induce adaptive immune response to generate activated T/B cells
or antibodies.
 Immunoreactivity: The ability of antigen to combine with activated T/B cells or antibodies.
Complete antigen(immunogen): be immunogenic and immunoreactive
Incomplete antigen (hapten): be only immunoreactive
Antigenic specificity
Epitope
 Definition of epitope: An epitope (or an antigenic determinant) is a particular chemical group of an antigen that
determines the specificity of an immune response, and is the specific site to which a given TCR/BCR or
antibody binds.
 Classification of epitope
Classification based on spatial stucture
sequential epitope: all of the amino acid residues that form a given epitope are covalently linked to
one another and are positioned sequentially in the linear sequence of a protein
conformational epitope: the epitope form only when the critical residues are brought together in space
through folding of the polypeptide chain into its normal three-dimensional conformation.
Classification based on cell type
B cell epitope: recognized by BCR
T cell epitope: recognized by TCR
Comparison of T cell epitope and B cell epitope
characteristics T cell epitope B cell epitope
receptor TCR BCR
MHC restriction yes no
chemical nature protein protein, LPS, polysaccharide
size 8-17 amino acid residues 5-15 amino acid residues
structure type linear linear; conformational
position anywhere surface
 Definition of Antigenic Valence: The total number of epitopes that can combine with antibodies in an antigen
is called antigenic valence.
 Common epitope and cross-reaction
The same or similar antigen epitope that is contained by different antigens is called common epitope. The reaction of
antibodies or activated lymphocytes with the same or similar epitope in different antigens is called cross-reaction.

Chapter 2 Factors Influencing Immunogenicity

Physicochemical and structural properties of antigens
Foreignness, chemical nature, molecular size, structure, conformation, accessibility, physical form.

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Effect of host
Genetics, age, sex, health state.
Mode of contact
Dosage, route, times, interval, adjuvant.

Chapter 3 Classification of Antigen

Classification Based on Requirement of T cells
 TD-Ag(thymus dependent antigen): Most protein antigens require antigen-specific T cells help to stimulate B cells
to generate antibodies. This type of antigen is called TD-Ag.
 TD-Ag(thymus independent antigen): Some antigens don’t require the presence of T cells to stimulate B cells.
This type of antigen is called TI-Ag.
Classification based on relationship with host
 Heterophilic antigen: Heterophilic antigen is a kind commom antigen which exists in human, animals
and microorganism, also named Forssman Ag.
Example: hemolytic streptococcus, cardiac muscle and kidney tissue.
 Xenogenic antigen: the antigen comes from different genus and generic.
Examples: pathogenic microorganism, plant protein, animal serum, heterogeneity organ implant
 Allogenic antigen: the specific antigen exists in different individual of same genus.
Examples: ABO blood type antigen, Rh antigen system, HLA.
 Autoantigen: Oneself component that can induce body to self immune response.
Examples: changed or decorated self-antigen, enshrouded or isolation antigen.
 Idiotypic antigen: the specific antigen exists in the V region of TCR, BCR or Ig, having unique amino acid
sequences and structures.
Classification based on source
 Endogenous antigen: The antigens that generated within the APC. (Viral proteins in virus-infected cells,
tumor antigens in tumor cells).
 Exogenous antigen: The antigens that are taken up by endocytosis. (Protein that are part of a microorganism or other
large particle engulfed through phagocytosis; smaller particles or individual proteins that bound to the cell surface
and then captured through receptor-mediated endocytosis; free, soluble proteins in the extracellular fluid that
imbibed nonspecifically during pinocytosis).

Chapter 4 Non-Specific Immunogical Stimulator

Superantigen(SAg)
Definition: SAg are some antigenic substances that can non-specifically activate massive(2%-20%)T cells with
extremely low concentration(1-10 ng/ml), and induce violent immune responses.
Adjuvant
Definition: Adjuvants are non-specific immunoenhancer that can especially enhance the intensity or modify the type of
immune responses to many antigens when administered before antigens or along with them.
Mitogen
Definition: Substance which can non-specifically activate polyclonal T cells or B cells ( or both ) by cross-linking
surface glycoproteins.

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Section 4 Antibody
Definition of antibody(Ab): Immunoglobulins produced by plasma cells which differentiated from B lymphocytes or
memory B cells in response to particular antigens, mainly exist in the serum or other kind of body fluids and function
as a cardinal kind of immune effectors.
Definition of immunoglubulin(Ig): Globulins which either function as antibodies or have the similar chemical
structures with antibodies.

Chapter 1 Organization of Ig
Basic molecular structure of Ig
 “Y” shape.
 The four-chain basic unit: 2 heavy chains & 2 light chains, held together by covalent interchain disulfide bonds
to form a bilaterally symmetrical structure.
 Heavy chain(H) and light chain(L)
classes of heavy chain: a g m d e
classes of Ab: IgA IgG IgM IgD IgE
types of light chain: k l
types of Ab: k l
 Variable region and constant region
1. Variable (V) region: in the N-terminal domain, vary widely, 1/2 light chain (VL) and 1/4 heavy chain(VH);
Constant (C)region: in the C-terminal domain, remain relatively constant, 1/2 light chain (CL) and 3/4 or 4/5 heavy
chain(CH).
2. Variable region includes framework region(relatively invariant) and hypervariable region(extremely variant).
3. Definition of HVR (CDR):VH and VL each contain three regions where the amino acid sequences are extrme
variability, these regions are called the hypervariable regions (HVR). Antigen binding is mediated by noncovalent
interactions that primarily involve the amino acids in HVRs of each chain; hence, the sequences of these regions
are the primary determinants of antibody specificity. So HVRs are also called complementarity-determining
regions (CDR), and within each chain are designated HVR1(CDR1), HVR2(CDR2), and HVR3(CDR3).
 Domian
L: VL CL; H: VH CH1 CH2 CH3 (CH4)
 Hinge region
1. Location: between the CH1 and CH2 domains of the heavy chains.
2. Composition: many proline residues.
3. Functions: permits flexibility between the two arms of antibody and allows the two arms to open and close to
accommodate binding to two epitopes; can be cleaved by proteases.
Other components of antibody
 Joining chain
 Secretory piece, SP

 Enzymatic digestion products of antibody

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papain pepsin
enzymatic on the N-terminal side of the inter- on the C-terminal side of the inter-
digestion location heavy-chain disulfides in hinge region heavy-chain disulfides in hinge region
2 Fabs F(ab)’2
• an entire light chain along with the VH and • ≈two disulfidelinked Fabs
enzymatic CH1 domains of one heavy chain • bivalent antigen-binding activity
digestion • monovalent antigen-binding activity
products Fc pFc’
of Ig • the C-terminal portions of both heavy chains • extensively degraded
held together by disulfides • usually doesn’t survive as an intact
• crystallizable fragment
• can be recognized by Fc receptors on
many types of cells
• determine many Ab’s secondary activities

Chapter 2 Diversity and immunogenicity of Antibody

Isotype; Allotype; Idiotype.

Chapter 3 Functions of Antibody

Antigen Recognition: specifically recognize and bind to antigens

 antibody
In vivo: neutralize toxins of microorganisms; prevent bacteria from adhering to host cells; neutralize viruses.
In vitro: immunodiagnosis.
 mIg: BCR(mIgM/mIgD), recognize antigens.
Complement activation
1. Antigen-bound IgM and IgG(IgG1, IgG2 and IgG3) can initiate the classical pathway of complement activation via
their CH3 or CH2 domain.
2. Polymers of IgG4, IgA and IgE can initiate the alternative pathway of complement activation.
Binding to Fc receptors
1. Opsonization: After binding to epitopes on bacteria via its Fab regions, IgG can bind to FcgR on macrophages or
neutrophils via its Fc region, and then enhances phagocytosis of the antibody-coated bacteria by phagocytes.
2. ADCC(antibody-dependent cell-mediated cytotoxicity): Antibody reacts with epitopes on virus-infected cells or
tumor cells via its Fab regions, and binds to FcR on killer cells(NK cells or macrophages) via its Fc region, and so
mediates the killing cells killing the antibody-coated target cells directly.
3. Involvement in typeⅠhypersensitivity: IgEs which are produced in response to an Ag bind to FceRⅠon mast cells
and basophils. When these cell-associated IgEs are cross-linked by the Ag, the cells are activated to release a
variety of mediators, and then induce typeⅠhypersensitivity.
Crossing the Placenta and Mucosa
1. Placental transfer: IgG is the only class of Ig that can cross the placenta in human, and it is responsible for
protection of the newborn during the first months of life.
2. Mucosal transfer: SIgA can cross the mucosa of respiratory and alimentary tracts, and participate local mucosal

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immune response.

Chapter 4 Biological Properties and Functions of Antibody Classes

IgG
 Major serum Ig;
 It is the most abundant antibody produced during secondary humoral immune response in the blood;
 IgG is the only class of Ab that can cross the placenta in human.
 Functions: opsonization,complement activation, ADCC;
IgM
 Two forms: mIgM and serum IgM;
 Serum IgM (macroglobulin):
1. A J-chain-containing pentamer, most molecular weight of antibodies;
2. The most efficient antigen-binding and complement-activation antibody;
3. First antibody produced of fetus;
4. Predominates in the early primary immune responses;
5. Antibodies to ABO blood type antigens in serum are IgMs.
 mIgM: monomer, BCR, expressed on the surfaces of immature and mature B cells.
IgA
 Two forms: serum IgA and secretory IgA;
 Serum IgA: monomer;
Secretory IgA(SIgA): dimer (with J chain and secretory piece); the major Ab produced by B cells in MALT and the
most abundant Ab class found in secretions which participate local mucosal immune response.
IgD
 Two forms: mIgD and serum IgD;
 mIgD: BCR; the expression of mIgD indicates maturity of B cells.
IgE
 The least common serum Ig;
 Binds to high-affinity Fc receptors on basophils and mast cell surfaces and induce type Ⅰ Hypersensitivity.
 Involved in the resistance to infection by parasites.

Chapter 5 Antibody Technology

Polyclonal antibody(pAb)
Monoclonal antibody(mAb): The homogeneous antibody produced by a hybridoma clone and recognize an epitope is
called a monoclonal antibody.
Genetic engineering antibody

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Section 5 The Complement System

Definition of the complement system
The complement system is a protein reaction system with precise regulation mechanisms that widely exist in serum,
tissue fluid and on the cell surface, including more than 30 kinds of components.

Chapter 1 Introduction

Components of complement system

 Complement innate component: C1-C9, MBL(mannose-binding lectin), MASP(MBL associated serine
protease), factor B, factor D, properdin(factor P);
 Complement regulatory protein: factor I, factor H, C1INH(C1 inhibitor), C4bp(C4 binding protein),
SP(S protein), DAF(decay-accelerating factor), MCP(membrane cofactor protein) etc;
 Complement receptor(CR): CR1-CR5, C3aR-C5aR, etc.

Chapter 2 Pathways of Complement Activation

Classical pathway
 Components: C1(C1q, C1r, C1s), C4, C2, C3, C5-C9
 Activator: antigen-antibody complex (immune complex, IC)
 Activation requisition:
1. Ab: only IgG1-IgG3(CH2), IgM(CH3);
2. The formation of Ag-Ab complex;
3. One C1 molecule should simultaneously bind to the Fc regions of 2 or more than 2 antibody molecules.
 Activation process:

Alternative pathway
 Components: C3, factor B, factor D, properdin(factor P), C5-C9
 Activator: certain bacteria, lipopolysaccharide(LPS), zymosan, polyglucosan, polymer of IgA/IgG4.
 Activation process:

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Alternative pathway of complement activation

MBL pathway
 Components: MBL or ficolin(FCN), MASP, C4, C2, C3, C5-C9
 Activator: certain carbohydrates(mannose) expressed on the surface of microorganisms.
 Activation process:

MBL pathway of complement activation

Terminal sequence
 Components: C5, C6, C7, C8, C9.
 Final product: MAC(membrane attack complex).
Emergence of three activation pathways in proper order:
alternative pathway → MBL pathway→ classical pathway
Three complement activation pathways:

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classical pathway
IC (IgG or IgM)

activated C1s

C4b2a C4b2a3b
(C3 convertase) (C5 convertase)
MBL pathway

mannose MASP2 MAC

MASP1

alternative C3bBb C3bBb3b

pathway B D (C3 convertase) (C5 convertase)

Complement activation pathways

Comparison of three complement activation pathways

classical pathway alternative pathway MBL pathway
activator Ag-Ab complex (IgG1- certain bacteria, LPS, zymosan, certain carbohydrates (mannose)
IgG3/IgM) polyglucosan, polymer of expressed on the surface of
IgA/IgG4 microorganisms
initial component C1 C3 MBL
components C1, C4, C2, C3, C5-C9 C3, factor B, factor D, factor P, MBL(FCN), MASP, C4, C2, C3, C5-
C5-C9 C9
need of Ab yes no no
C3 convertase C4b2a C3bBb C4b2a
C5 convertase C4b2a3b C3bBb3b C4b2a3b
assists Ab to generate takes part in the innate takes part in the innate immunity, plays
biological immune effects, plays role immunity, plays role in the role in the early stage of infection or
activity and in the later or recovery initial stage of infection or primary infection, promotes classical
characteristics stage of infection, and primary infection, has a positive and alternative pathways.
resists secondary infection feedback loop.
of the same pathogen.

Chapter 3 Regulation of Complement Activation

Regulatory Mechanisms for Front-end Reaction of Classical Pathway: C1INH, CR1, C4bp, DAF, MCP, factor I;
Regulatory Mechanisms for Front-end Reaction of Alternative Pathway: CR1, DAF, MCP, factor I, factor H, factor P
Regulatory Mechanisms for MAC: MIRL, HRF(C8bp), SP, clusterin.

Chapter 4 Biological Consequences of Complement System

Biological functions of complement System

 Cell lysis: Generally the lytic funciton of complement system is equated to the membrane attack complex(MAC)
lesions.
 Lysis of bacteria, viruses and parasites
 Lysis of tumor cells
 Lysis of self-cells in pathological conditions

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 Opsonization: After binding to the surfaces of bacteria or other particulate substances, C3b, C4b and iC3b fragments
of complement activation can be recognized by relevant complement receptors on phagocytes, and then enhances
phagocytosis of these complement-coated substances.
 Mediators of Inflammation
1. Anaphylatoxin: C3a,C5a and C4a cause degranulation of mast cell and basophil by binding to relevant receptors on
these cells, with consequent release of histamine and other bioactive substance that induce inflammation;
2. Chemotaxis: C5a is strongly chemotactic for neutrophils, inducing their migration toward the site of inflammation.
 Clearance of Immune Complex(Immune adherence): The C3b-coated immune complex is able to bind to CR1 of
erythrocyte or platelet which carrys the immune complex to the liver and spleen where it is ingested by macrophage.
Pathophysiological significances of complement activation
 Anti-infection defense
 Participate in the adaptive immune response;
 Interaction with other cascade reaction systems.

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Section 6 Cytokine
Definition of cytokine: Cytokines are a diverse group of micro-molecule soluble polypeptides which secreted by a
variety of immune cells and histiocytes and play regulatory roles between cells. They regulate the growth,
differentiation and effects of target cells and control immune responses through the combination of the corresponding
receptors.

Chapter 1 General Properties of Cytokines

Essential features of cytokines

 Low molecular weight proteins;
 Soluble;
 High efficiency: cytokines have biological activities even in low concentration;
 Cytokines act by binding to high-affinity surface receptors on target cells;
 Inducible;
 Short half-life;
 Most of cytokines act only locally over short distances.
Manners of cytokine action
 autocrine manner: act on the producing cell itself;
 paracrine manner: act on adjacent cells;
 endocrine manner: act on distant target cells.
Functional characteristics of cytokines
 Pleiotropism
 Redundancy
 Synergy
 Antagonism
 Network

Chapter 2 Classification of Cytokines

Interleukin(IL)
Colony-stimulating factor(CSF)
 Definition: CSFs are cytokines that stimulate the differentiation and proliferation of pluripotential hemopoietic stem
cells or hemopoietic progenitor cells of different developmental stages in the bone marrow.
 Classification: macrophage-CSF(M-CSF), granulocyte-CSF(G-CSF), GM-CSF, stem cell factor(SCF),
erythropoietin(EPO), thrombopoietin(TPO) etc.
Interferon(IFN)
 Definition: IFNs are glycoproteins which are secreted by leukocytes, T lymphocytes, NK cells and other cell types in
response to viruses or interferon inducers, and can interfere with viral infection and replication.
 Classification:
typeⅠ: IFN-a and IFN-b, mainly produced by virus-infected cells.
typeⅡ: IFN-γ, mainly produced by activated T cells and NK cells.
 Functions: antiviral, antiproliferative, antineoplastic and immunomodulatory effects.
Tumor necrosis factor(TNF)
 Definition: TNFs are cytokines which can induce hemorrhagic necrosis of tumors.
 Classification:

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TNF-a: also known as cachectin, produced by activated macrophage;

TNF-b: also known as lymphotoxin(LT), mainly produced by activated T cells.
 Functions: modulation of immune response, killing target cells, induction of cell apoptosis..
Growth Factor(GF)
TGF-β, VEGF, EGF, FGF etc
Chemokine.

Chapter 4 Immunological Functions of Cytokines

Regulation of the development, differentiation, and functions of immune cells

 Regulation of immune cells development and differentiation in central immune organs;
 Regulation of immune cells development, differentiation, activation and functions in peripheral immune organs.
Regulation of immune responses
 Anti-infective effects (antibacterial immunity and antiviral immunity);
 Antineoplastic effects;
 Induction of cell apoptosis;
 Negative regulation of immunity.

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Section 7 Leukocyte Differentiation Antigens and Adhesion Molecules

Chapter 1 Human Leukocyte Differentiation Antigens

Definition of human leukocyte differentiation antigen: Human leukocyte differentiation antigens are cell surface
molecules which express on cell membrane when stem cells differentiate into different lineage cells or when blood
cells are in maturational stages and activation status．
Definition of CD(cluster of differentiation): All of the monoclonal antibodies from different laboratories that react with
a particular differentiation antigen are grouped together as a cluster of differentiation (CD). CD is nomenclature of
human leukocyte differentiation antigens.

Chapter 2 Adhesion Molecules

Definition of CAM(cell adhesion molecules): the molecules that mediate contacting and binding between cells or
between cells and extracellular matrix are referred to as cell adhesion molecules.
Mode of action: CAMs play roles in the form of receptor-ligand binding.
Classification: immunoglobulin superfamily, integrin family, selectin family, cadherin family, etc
Functions of cell adhesion molecules
 Participating in the interaction and activation of immune cells;
 Participating in the adhesion of leukocytes with vascular endothelial cells during the inflammatory response;
 Lymphocyte homing.

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Section 8 Major Histocompatibility Complex

Definition of MHC(major histocompatibility complex): MHC is an extended genetic locus, containing a group of
closely-linked genes, which determines whether transplanted tissue is histocompatible, and is closely related to
immune response.
In human MHC is referred to as HLA(human leukocyte antigen) gene complex, the products are called HLA molecules
(HLA antigens)

Chapter 1 Structure and Genetic Properties of HLA

 HLA gene complex

 Localization: on the short arm of chromosome 6.
 Classical classⅠgenes: include HLA-B, -C, -A loci, encode a chain of HLA classⅠmolecule.;
 Classical classⅡgenes: include HLA-DP,DQ,DR regions, encode a chain and b chain of HLA classⅡmolecule.
Genetic properties of human MHC
 Polymorphism
 Linkage disequilibrium and haplotype

Chapter 2 Products of Human MHC: HLA Molecules

Distribution of HLA Molecules

 HLA classⅠmolecules expressed on the surface of all nucleated cells.
 HLA classⅡmolecules expressed on the surface of professional antigen presenting cells(dendritic cells, macrophages
and B cells), thymic epithelial cells and activated T cells.
HLA classⅠmolecules
 Structure of HLA classⅠmolecules
1. Heavy chain (αchain): encoded by classical classⅠgenes (HLA-B/C/A) on chromosome 6; transmembrane
polypeptide containing three extracellular domains (α1、α2 andα3).
2.β2 microglobulin (β2m): encoded by a gene on chromosome 15; with one extracellular domain.
 Structural Regions of HLA classⅠmolecules
1. peptide-binding region
①α1 andα2 domains;
②binds endogenous antigenic peptides;
③the end is closed and it can bind peptides of 8-10 amino acids.
④determine the polymorphism of HLA classⅠmolecules.
2. Ig-like region
①α3 domain andβ2m;
②secondary structure is Ig fold;
③highly conserved among HLA classⅠmolecules, nonpolymophic;
④β2m stabilizes the class Ⅰ molecules and facilitates its expression on cell membranes;
⑤α3 domain is a CD8-binding site.
3. transmembrane region: anchors HLA classⅠmolecule on membrane.
4. cytoplasmic region: signal transduction.
HLA classⅡmolecules
 Structure of HLA classⅠmolecules

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αchain and βchain: both encoded by classical classⅡgenes (HLA-DP/DQ/DR) on chromosome 6 transmembrane
polypeptides; each containing two extracellular domains(α1 and α2 or β1 and β2)
 Structural Regions of HLA classⅡmolecules
1. peptide-binding region
①α1 and β1 domains;
②binds exogenous antigenic peptides;
③the end is more open and it can bind peptides of 13-17 amino acids.
④determine the polymorphism of HLA classⅡmolecules.
2. Ig-like region
①α2 domain andβ2 domain;
②secondary structure is Ig fold;
③highly conserved among HLA classⅡmolecules, nonpolymophic
④β2 domain is a CD4-binding site.
3. transmembrane region:anchors HLA classⅡmolecule on membrane.
4. cytoplasmic region: signal transduction.
Comparison of HLA classⅠand classⅡmolecules
HLA classⅠmolecules classⅡmolecules
genes HLA-B, C, A HLA-DP, DQ, DR
structure αchain,β2m αchain,βchain
peptide-binding region α1+α2 (closed) α1+β1(open)
distribution all nucleated cells APC, activated T cell
characteristic of expression codominance codominance
major functions presents the endogenous antigenic presents the exogenous antigenic
peptides to CD8+T cell peptides to CD4+T cell
Peptide-HLA Molecule Interaction
 Molecular Basis: The peptide-binding groove of HLA molecules interact with the anchor residues of antigenic
peptide;
 Anchor position: The polymorphic residues of HLA chains form several pockets in the peptide-binding groove and
are responsible for determining the structure of peptides which may be accommodated, these pokets are called
anchor positions;
 Anchor residue: The amino acid residues at the defined positions along the antigenic peptide which anchor the
peptide into the anchor positions in the peptide-binding groove of HLA molecule are called anchor residues.
 Consensus motif
 Characteristics of Peptide-HLA Molecule Interaction: specificity, flexibility
Functions of HLA Molecules
 Participate in adaptive immune responses as antigen-presenting molecules.
(1)MHC restriciton;
①Definition of MHC restriction: T cells achieve dual recognition of the antigenic peptides and self MHC molecules
through their TCRs, that means any individual’s T cells only recognize foreign antigenic peptides presented by the
MHC molecules of that individual.
②CD8+T cells recognize endogenous antigenic peptides bound to classⅠMHC molecules and are called classⅠ
restricted; CD4+T cells recognize exogenous antigenic peptides bound to classⅡMHC molecules and are called
classⅡrestricted.

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 Medical Immunology

(2)Participate in the selection and differentiation of T cells in thymus;

(3)Determine the individual difference of disease susceptibility;
(4)Involved in genetic structure heterogeneity of population.
 Participate in innate immune responses as regulatory molecules
(1)Classical class Ⅲ genes encode complement components;
(2)Products of nonclassical classⅠgenes and MICA gene regulate the activity of NK cells and part of killer cells;
(3)Inflammation related genes initiate and regulate inflammatory reactions, and play roles in stress reactions.

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Section 9 B Lymphocytes
Chapter 1 Development of B Lymphocytes

Gene structure and rearrangement of BCR

 Germline gene structure of BCR
1. The genes encoding H chain: V gene segment (VH), D gene segment (DH), J gene segment (JH) and C gene
segment (CH); on chromosome 14;
2. The genes encoding L chain: V gene segment (Vκ/Vλ), J gene segment (Jκ/Jλ) and C gene segment
(Cκ/Cλ); on chromosome 2 (κ) and chromosome 22 (λ).
 Definition of allelic exclusion: The successful rearrangement of heavy-or light-chain genes on one chromosome
prevents all other genes on another homologous chromosome from undergoing rearrangement in the same cell, and
consequently makes sure that only one heavy chain and one light chain to be expressed in any individul B
lymphocyte.
 Definition of isotypic exclusion: The successful rearrangement of κlight-chain genes prevents l light-chain genes
from undergoing rearrangement in the same cell, and consequently makes sure that only one type of light chain to be
expressed in any individul B lymphocyte.
Generation mechanisms of BCR diversity
 Combinational diversity;
 Junctional diversity;
 Receptor editing;
 Somatic hypermutation.
The B cells development in the central Immune organ
 Position: bone marrow
 Stages: pro-B cell; pre-B cell; immature B cell; mature B cell.
 Results: generation of BCR; self tolerance.
Central tolerance of B lymphocytes
Clone deletion, receptor editing, anergy.

Chapter 2 Surface Markers of B Lymphocyte

B cell receptor complex (BCR complex)

 mIg(BCR, B cell receptor)
1. Structure: transmembrane protein of two identical heavy chains and two identical light chains; monomer.
2. Function: recognizes and binds specific antigen
 Igα(CD79a)/Igβ(CD79b)
1. Structure: heterodimer of Iga (CD79a) and Igb (CD79b); noncovalently associate with BCR to form the BCR
complex; transmembrane glycoproteins with ITAM in each cytoplasmic domain
2. Function: transmits the first signal of B cell activation into the cell.
Coreceptor
 CD19/CD21/CD81 complex;
 CD19 is a signaling molecule;
 CD21 is the complement receptor 2 (CR2) that can bind C3d, and is the receptor for EB virus;
 Functions: enhances the recognition of antigen by B cell and promotes the B cell activation.
Co-stimulatory molecules

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 CD40: expressed on the mature B cell surface, binds to CD40L expressed on activated Th cells, delivers the most
important second signal of B cell activation.
 CD80(B7.1)/CD86(B7.2)
1. expressed on the activated B cell surface
2. interact with CD28 on naive T cell surface, deliver the most important second signal of T cell activation;
3. interact with CTLA-4 on activated T cell surface, deliver co-inhibitory signal to inactivate the responding T cell.
 Adhesion molecule(LFA-1, ICAM-1): mediate contacting and binding between T cells and B cells, also deliver
co-stimulatory signal.
Double Signals for B Cells Activation
 The first signal (the antigen signal, the BCR signal): produced by the recognition of antigen by the BCR;
transimitted by Igα(CD79a)/Igβ(CD79b) and coreceptor (CD21/CD19/CD81)
 The second signal (co-stimulatory signal): co-stimulatory molecules, (B) CD40←CD40L (Th)

Chapter 3 Subsets of B Lymphocytes

B-1 cell (CD5+): participates innate immunity;

B-2 cell (conventional B cell, CD5-): participates adaptive immunity.

Chapter 4 Functions of B Lymphocytes

Mediate humoral immunity by producing antibodies

neutralization, opsonization, ADCC, activating complement, participating typeⅠhypersensitivity
Antigen presentation: activated B cells as professional APC, especially important for the presentation of soluble
Antigens.
Immunoregulation function

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Section 10 T Lymphocytes
Chapter 1 T Lymphocytes Ontogeny

Development of T lymphocytes in the thymus

 Stages: (1)pro-T cell→pre-T cell→immature T cell →mature T cell
(2)double negative stage→double positive stage →single positive stage
 Process: rearrangement of the TCR genes; positive selection; negative selection
 Results: expression of TCR; self-MHC restriction; self-immunological tolerance
 Process:
1. Rearrangement of the TCR genes
1)Location: in the thymic cortex.
2)Stages: DN stage→DP stage.
3)Process:
DN stage: rearrangement of the TCR b gene in pro-T cells, expression of the pre-TCR (pTa:b) on pre-T cells;
DP stage: rearrangement of the TCR a gene, expression of an baTCR on immature T cells.
4)Result: express functional TCR.
2. Positive selection
1)Location: in the thymic cortex.
2)Stage: DP stage.
3) Process:

4)Result: acquire self-MHC restriction.

5)Definition of positive selection: In the thymic cortex, double positive cells whose TCRs are able to recognize
peptide-self-MHC complexs expressed on thymic epithelial cells with proper affinity will survive and differentiate
into single positive cells (recognize classⅠMHC molecules differentiate into CD3+CD4-CD8+SP cells/recognize
classⅡMHC molecules differentiate into CD3+CD4+CD8-SP cells), those unable to recognize or recognize with high
affinity will die by apoptosis. T cells aquire self-MHC restriction via positive selection.
3. Negative selection
1)Location: in the cortico-medullary junction and thymic medulla.
2)Stage: SP stage.
3)Process:

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4)Result: acquire self-immunological tolerance.

5)Definition of negative selection: Single positive cells that recognize self-peptide-MHC complexs expressed on
thymic dendritic cells and macrophages in the cortico-medullary junction and thymic medulla with high affinity
will undergo apoptosis, those unable to recognize or recognize with low affinity will survive and undergo
maturation. T cells acquire self-immunological tolerance via negative selection.
Development of T lymphocyte in the peripheral immune organ

Chapter 2 Surface Proteins of T Lymphocytes

TCR-CD3 complex
 T Cell Receptor (TCR)
1. Structure: a heterodimer composed either of a and b chains (95%-99%) or of g and d chains(1%-5%);
contain V region and C region.
2. Function: TCRba recognizes peptide-MHC complex (pMHC), dual specificity, MHC restriction.
 CD3:
1. Structure: a complex of three dimers (γε, δε, ζζ or ζη); noncovalently associate with TCR to form the
TCR-CD3 complex; transmembrane proteins with ITAM in each cytoplasmic domain
2. Function: transmits the first signal of T cell activation into the cell.
CD4 and CD8(coreceptor)
 CD4
1. Structure and distribution: a single-chain transmembrane protein; expressed on 60%-65% of baT cells and partial
NKT cells;
2. Functions:
(1)increases the interaction between T cell and APC by binding to b2 domain of MHC classⅡmolecule, and helps
the recognition of exogenous antigen by TCR, and promotes the generation of the first signal of T cell activation;
(2)participates in the transduction of first signal for activation;
(3)receptor of HIV gp120.
 CD8
1. Structure and distribution: a transmembrane heterodimer of a and b chain; expressed on 30％-35％ of ba T cells
and partial dg T cells;
2. Functions:
(1)increases the interaction between T cell and APC by binding to a3 domain of MHC classⅠmolecule, and helps
the recognition of endogenous antigen by TCR, and promotes the generation of the first signal of T cell
activation;

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(2)participates in the transduction of first signal for activation.

Costimulatory molecules
 CD28
1. Structure and distribution: a transmembrane homodimer; expressed on 90% of CD4+T cells and 50% of CD8+T
cells;
2. Function: binds to CD80 (B7-1) and CD86 (B7-2) expressed on the professional APCs, delivers the most
important second signal of T cell activation.
 CTLA-4(cytotoxic T lymphocyte antigen-4, CD152)
1. Distribution: expressed on activated CD4+ and CD8+ T cells;
2. Function:
(1)binds to CD80 (B7-1) and CD86 (B7-2) expressed on the professional APCs with higher affinity than CD28;
(2)has ITIM in its cytoplasmic domain and delivers inhibitory signal to down regulate or terminate T cell
activation.
 CD40L(CD154)
1. Distribution: expressed on activated CD4+T cells;
2. Functions:
(1)binds to CD40 on APCs and promotes APCs activation;
(2)the expression of B7 molecules and the secretion of cytokines by APCs increase after activation, which in turn
promotes T cell activation;
(3)binds to CD40 expressed on B cells, delivers the most important second signal of B cell activation.
Double signals for T cells activation:
 The first signal (antigen signal, TCR signal): produced by the recognition of peptide-MHC complex by the TCR;
transimitted by CD3 and coreceptor (CD4/CD8)
 The second signal (co-stimulatory signal): co-stimulatory molecules, (T) CD28-CD80(B7-1)/CD86(B7-2) (APC)

Chapter 3 T lymphocytes subsets and functions

 Classification based on activation status: naïve T cell; effector T cell; memory T cell.
Classification based on TCR types: ab T cell; gd T cell.
Classification based on CD molecules: CD4+T cell; CD8+T cell.
Classification based on functional features: helper T cell (Th), cytotoxic T cell (CTL), regulatory T cell (Treg)
 Helper T cell(Th)
1. Subsets of CD4+Th
(1)Th1: IL-2, IFN-γ, TNF;
(2)Th2: IL-4, IL-5, IL-6, IL-10, IL-13;
(3)Th3: TGF-β;
(4)Th17: IL-17.
(5)Tfh: IL-21
2. Regulation of CD4+Th differentiation

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cellular immunity

IFN-γ

humoral immunity

3. Functions of CD4+Th subsets

(1)Functions of Th1 cells: promotes celluar immunity.
Secrete Th1-type cytokines (IFN-g, TNF, IL-2, etc), enhance cell-mediated anti-infection immunity, especially the
resistance to infections of intracellular pathogens.
1)IFN-g activates macrophages, induces Ig class switching to IgG;
2)IL-2, IFN-g, IL-12 enhances killing ability of NK cells;
3)IL-2, IFN-g promote proliferation and differentiation of CTL；
4)TNF induces target cell apoptosis, promotes inflammation；
5)Participate in type Ⅳ hypersensitivity and certain autoimmune disease.
(2)Functions of Th2 cells: promotes humoral immunity.
Secrete Th2-type cytokines (IL-4, IL-5, IL-6、IL-10, IL-13, etc).
1)Help humoral immunity：promote the activation, proliferation and differentiation of B cells and the generation of
antibodies by secreting IL-4, IL-5, IL-6 and IL-10;
2)Involved in hypersensitivity inflammation: induce B cells class switching to IgE and eosinophils activation by
producing IL-4 and IL-5, participate in typeⅠhypersensitivity and the resistance to parasitic infections.
 Cytotoxic T cell (CTL)
1. Function: recognize endogenous antigenic peptide-MHC class I molecule complex specifically, kill the target cells
(including virus-infected cells, intracellular microorganism-infected cells, tumor cells).
2. Characteristics: antigenic specificity, MHC restriction, continuous killing.
3. Mechanisms:
(1)perforin/granzyme pathway: kill target cells by secreting perforin, granzyme, granulysin and LT;
Perforin is a pore-forming protein monomer in the granules of CTLs. Perforin polymerizes and forms an aqueous
channel on the target cells. Then the target cells die because osmotic swelling;
Granzymes enter the target cells through these aqueous channels formed by perforin. They activate caspases and
induce target cells apoptosis.
(2)Fas-FasL pathway:
CTLs express FasL, that binds to its target protein Fas, which is expressed on target cells. This interaction results
in activation of caspases and apoptosis of target cells.

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Section 11 Antigen-Presenting Cells

and Antigen Processing and Presentation

Chapter 1 Types and Characteristics of antigen-presenting cells

Definition of antigen-presenting cell(APC): The cells that can process antigens and present antigenic peptides to T cells in
the form of peptide-MHC complex are named as antigen-presenting cells (APCs), which play important roles in immune
recognition, immune response and immune regulation.
Classification of APCs
 APCs that present exogenous antigens by class Ⅱ MHC molecules(present the antigens to CD4+T cells)
According to their ability to express classⅡMHC molecules and costimulatory molecules:
1.Professional APCs: dendritic cells, macrophages and B lymphocytes; constitutively express class Ⅱ MHC
molecules, co-stimulatory molecules and adhesion molecules, have the functions of antigen capture, processing and
presentation.
2.Non-professional APCs: endothelial cells, epithelial cells, fibroblasts, etc; can be induced to express class Ⅱ MHC
molecules, co-stimulatory molecules and adhesion molecules, have weaker abilities of antigen processing and
presentation.
 APCs that present endogenous antigens by class Ⅰ MHC molecules(present the antigens to CD8+T cells)
1.Intracellular pathogen-infected cells which produce pathogen antigens: virus-infected cells, intracellular
microorganism-infected cells.
2.cells undergo mutation which produce mutant protein antigens: tumor cells
Professional APCs
 Dendritic Cells (DCs)
1. Introduction:
(1)The morphological feature of mature DC is that it is covered with long membrane dendrite-like extensions;
(2)DCs are the most potent APCs known;
(3)DCs are extremely efficient at capturing and presenting antigens and at activating naïve T cells;
(4)DCs are responsible for initiating most acquired immune response, and have a key role in integrating innate and
acquired immunity.
2. Classification of DCs:
(1)Based on the sources: conventional DC (cDC)(myeloid DC), plasmacytoid DC (pDC)(lymphoid DC);
(2)Based on the mature status: imature DC, mature DC.
3.cDC matuaration process: imature DC→migration stage DC→mature DC
(1)Immature DC: express numerous receptors (Fc receptors, mannose receptors) but very little classⅡMHC
molecules and co-stimulatory molecules; its principal function is antigen capture and processing.
(2)Mature DC: strongly express classⅡMHC molecules and co-stimulatory molecules; its principal function is
antigen presentation to T cells.
4. Functions of DCs:
(1)Antigen recognition, capture and processing, and participate in innate immunity;
(2)Antigen presentation and immune activation;
(3)Immunoregulation;
(4)Immunological tolerance induction and maintenance
 Monocytes/Macrophages
 B Lymphocytes

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Chapter 2 Antigen Processing and Presentation

Classification of antigens:
 exogenous antigen: taken up by endocytosis(cells, bacteria, protein antigens), presented with classⅡMHC molecule to
the CD4+T cell.
 Endogenous antigen: generated within the APC (viral proteins in virus-infected cells, tumor antigens in tumor cells,
self-antigens in certain cells), presented with classⅠMHC molecule to the CD8+T cell.
Pathways of antigen processing and presentation
 ClassⅠMHC molecule pathway (endogenous antigen presenting pathway);
 ClassⅡMHC molecule pathway(exogenous antigen presenting pathway);
 Non-classic antigen presenting pathway;
 CD1 related antigen presenting pathway.
ClassⅠMHC molecule pathway (endogenous antigen presenting pathway)

1. Endogenous antigens bind to ubiquitins;

Ag 2. Ubiquitinated proteins are degraded into short peptides by proteasome in cytoplasm;
3. Selected peptides are pumped into the lumen of rough endoplasmic reticulum (RER) by TAP

Peptide-classⅠMHC complexs are delivered to the cell surface for presentation to CD8+T cells.
Class Ⅰ MHC2. a chain and b2m are assembled to form class I MHC molecule.
Molecule 1. In the RER lumen, the a chains of classⅠ MHC molecules bind to chaperones (calnexin, tapasin) immediately
Class Ⅰ after synthesis;
MHC
Mole
 Proteasome
1. Large, multi-subunit enzyme assemblage.
2. The core components are proteasome subunit beta type 8 and 9 (PSMB 8 and PSMB 9) or low molecular weight
peptide (LMP2 and LMP9);
3. Degrades a broad range of cytosolic proteins
 TAP (transporter associated with antigen processing)
1. A heterodimer of TAP1 and TAP2;
2. Form a channel that selectively pumps peptides of 8-12 amino acid residues from the cytoplasm into the RER
lumen in an ATP-dependent manner.
ClassⅡMHC molecule pathway(exogenous antigen presenting pathway)

1.Exogenous antigens are captured by APC and taken into the cell, merge with endosomes or form phagosomes;
Ag 2. Phagosomes and lysosomes merge into phagolysosomes;
3. endosomes or phagolysosomes merge with MⅡC;
4. Exogenous antigens are degraded into peptides in phagolysosomes and MⅡCs.

Peptide-classⅡ complexs are delivered to the cell surface for presentation to CD4+T cells
4. CLIP is catalytically removed by the HLA-DM molecule.
3. Ii is partially cleaved in MⅡC and leave a classⅡ-associated invariant chain peptide (CLIPs) in the peptide-
Class Ⅱ MHC binding groove.
Molecule 2. Vesicles bearing class Ⅱ/Ii nonamers enter into the cytoplasm from the RER, and form MHC classⅡ
Class Ⅰ compartments (MⅡCs);
MHC 1. Class Ⅱ MHC molecules synthesized in the RER associate with Ia-associated invariant chains(Ii) to form
Mole (baIi)3 nonamers.

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 Ia-associated invariant chain (Ii)

1.Promote the assembling , folding and dimer-formation of class Ⅱ MHC molecules;
2.Block class Ⅱ MHC molecules binding endogenous antigenic peptides in the RER;
3.Promote the transportation of class Ⅱ MHC molecules to the MⅡCs.
 HLA-DM molecule
1. Encoded by MHC;
2. Catalytically remove the CLIP peptide;
3. Modulated by HLA-DO molecule.

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Section 12 Adaptive Immune Response Mediated by T Lymphocytes

cellular immune response may be divided into three phases
recognition → activation, proliferation and differentiation → effector

Chapter 1 T Cells Recognition of Antigens

T cell recognition of antigen has a dual specificity

 Antigen specificity;
 MHC restriction: T cells achieve dual recognition of the antigenic peptides and self MHC molecules through their
TCRs, that means any individual’s T cells only recognize foreign antigenic peptides presented by the MHC
molecules of that individual.
Antigen presentation
 Exogenous antigen presented with classⅡMHC molecule to the CD4+T cell
 Endogenous antigen presented with classⅠMHC molecule to the CD8+T cell
Interactions between APC and T cell
 Non-specific combination between APC and T cell
1. Adhesion molecules (LFA-1, CD2) on T cells bind to corresponding ligands (ICAM-1, LFA-3) on APCs;
2. Reversible and temporal, enhance the recognition of antigenic peptides by TCRs
 Specific combination between APC and T cell
1. TCR recognizes specific peptide-MHC complex;
2. CD3 transmits the specific antigen signal;
3. CD4/CD8 is the coreceptor which promote the generation and transduction of the first signal for T cell activation;
4. Costimulatory molecules (CD28/B7 ， LFA-1/ICAM-1, LFA-2/LFA-3) mediate contacting and binding between T
cell and APC, also deliver co-stimulatory signal.

Chapter 2 T cell Activation, Proliferation and Differentiation

T cell activation
 The first signal (antigen signal): The first signal for T cell activation is produced by the specific recognition of
peptide-MHC complexes by the TCR. The signal is transmitted into T cell by CD3 and CD4/CD8.
 The second signal (co-stimulatory signal): The second signal for T cell activation is produced by the interaction of
co-stimulatory molecules between T cell and APC.
T cell APC
CD28 B7-1/B7-2（CD80/86)
LFA-1 ICAM-1
LFA-2 LFA-3
 Cytokines: Cytokines are produced by activated APCs and T cells, and promote the proliferation and differentiation
of activated T cells(IL-1、IL-2、IL-6、 IL-12、IFN-γ)
Signals transduction and target genes of T cell activation
T Cells Proliferation and Differentiation
Cytokines: IL-2.
 Proliferation and differentiation of CD4+ T cell

IL-21,IL-6
Tfh

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IL-12, IFN-γ
Th1
IL-4
Th2
CD4+T TGF-β, IL-6, IL-23
Th17

TGF-β, IL-10, IL-4 Th3

Tm

 Proliferation and differentiation of CD8 T cell
+

CTL
+
CD8 T cell Tm

Chapter 3 Immunological Effects and Outcome of T cells

 Immunological effects of Th
 Effects of Th1
Induce CTLs differentiation via direct contact; Recruit and activate monocytes/macrophages and lymphocytes via
secreted cytokines to induce cellular immune response (mononuclearcells infiltration-based inflammatory reaction or
delayed-type inflammatory reaction)
1.To macrophages:
1)Activate macrophages (to defend against infections of intracellular pathogens):
①Produce INF-γand express CD40L to activate macrophages;
②Activated macrophages express high level of B7 and MHC classⅡmolecules and secrete IL-12 to amplify the
effects of Th1 response.
2)Induce and recruit macrophages:
①Produce IL-3 and GM-CSF to induce the generation of macrophages;
②Produce TNF-α, LTα and MCP-1 to recruit macrophages.
2.To lymphocytes:
1)Produce IL-2 to promote activation and proliferation of Th1, Th2, CTL and NK cells to amplify immunological
effects;
2)Produce IFN-γto promote B cells to generate antibodys (IgG) which have opsonization activity, and enhance
phagocytosis of macrophages.
3.To neutrophils:
1)Produce LT and TNF-αto activate neutrophils, and promote them to kill pathogens.
 Effects of Th2
1.Help humoral immune response: secrete IL-4, IL-5, IL-10 and IL-13 to help and promote the activation,
proliferation and differentiation of B cells and the generation of antibodies;
2. participate in hypersensitivity inflammation: secret IL-4 and IL-5 to activate mast cells, basophiles, eosinophils,
and participate in typeⅠhypersensitivity and the defense agaist parasitic infections.
 Effects of Th17
Participate inflammation and play role in innate immunity by secreting IL-17, IL-22 and IL-21.
 Effects of Tfh
Help B cells survival and proliferation in the germinal center, and promote the differentiation of B cells into plasma

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cells, antibody class switching and affinity maturation by the secretion of IL-21 and the expression of CD40L and
ICOS.
Immunological effects of CTL
 Function: kill the specific target cells including virus-infected or intracellular microorganism-infected cells and tumor
cells.
 Procedure:
1. Combination of effector cells and target cells;
2. Polarization;
3. Lethal hit.
 Mechanisms of CTLs’ killing
1. Perforin/granzyme pathway:
1) Perforin is a pore-forming protein monomer in the granules of CTLs. Perforin polymerizes and forms an aqueous
channel on the target cells. Then the target cells die because osmotic swelling;
2) Granzymes enter the target cells through these aqueous channels formed by perforin. They activate caspases and
induce target cells apoptosis.
2. Death receptor pathway: CTLs express FasL or secrete TNF-α, that bind to their target protein Fas or TNFR, which
are expressed on target cells. These interaction result in activation of caspases and apoptosis of target cells
Outcome of activated T cells
 Inhibition or elimination of effector T cells
1. immunosuppression function of Tregs
2. activation-induced cell death(AICD): refers to a spontaneous cell apoptosis that is induced after immue cells
activation and playing immune effects. Activated T cells express increased Fas which bind to FasL expressed on
multiple types of cells.This interaction results in activation of apoptotic signals in activated T cells and induce cell
apoptosis.
 Formation of memory T cells
1. Tms are long-lived T cells which have memory to the specific antigens;
2. Surface phenotype: CD45RA-CD45RO+
3. Participate the secondary response, result in a prompter and more effective immune response

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Section 13 Specific Immune Response Mediated by B Lymphocytes

Chapter 1 B Cell Response to TD-Ag

Antigen recognition of B cells
 B cell recognizes and binds an antigen in its free, unprocessed form through BCR.
1.Produces the first signal for B cell activation;
2.Takes up antigen by the BCR-mediated endocytosis and presents peptide-classⅡMHC complex to the CD4+T cell.
 No MHC restriction.
Signals for B cell activation
 The first signal (antigen signal)
1.The first signal for B cell activation is produced by the specific recognition of antigen by the BCR;
2.The signal is transmitted into T cell by Iga/Igb;
3.The coreceptor CD21/CD19/CD81 enhance the sensitivity of B cell to antigen stimulation, and promote the
transduction of activation signal.
 The second signal (co-stimulatory signal)
The second signal for B cell activation is produced by the interaction of co-stimulatory molecules between B cell
and Th.
B cell Th
CD40 CD40L
ICAM-1 LFA-1
 Cytokines promote B cell proliferation and differentiation
Cytokines produced by activated Th cells (Th2 and Tfh), such as IL-4 、IL-5、IL-21, promote the proliferation and
differentiation of activated B cells.
Signals transduction of B cell activation
Interaction between Th and B cells
 Activated Th cells help B cell mediated immune response
1.Co-stimulatory molecules expressed on activated Th cells deliver the second signal for B cell activation
(CD40L/CD40);
2.Cytokines secreted by activated Th cells promote the activation, proliferation and differentiation of B cells (Th2: IL-
4, IL-5, IL-6; Tfh, IL-21, etc).
 Activated B cells function as APC to activate T cells
1.B cells provide the first signal for T cell activation (peptide-class ⅡMHC complex);
2.Activated B cells provide the second signal for T cell activation (B7/CD28, etc).
Proliferation and terminal differentiation of B cells in germinal center
 Somatic hypermutation
1.Definition: With the stimulation of antigen and the help of Th cells, the variable region genes of heavy chains and
light chain in centroblasts undergo point mutation at an unusually high rate, this phenomenon is termed somatic
hypermutation;
2.Characteristic: The Ig V-region mutation rate is 10-3 / base pair/ cell division;
3.Results: form the BCR diversity and the antibody diversity in humoral immunity; affinity maturation.
 Affinity maturation
Definition: When a large amount of antigens are cleared, or in secondary response, antigen selects the B cells with
hihger affinity BCRs to proliferate and ultimately produce antibodies with high affinity.
 Ig class switching

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 Medical Immunology

1.Definition: Each mature B cell, after activation, initially expresses IgM antibodies and then undergoes switching to
a different class of antibody (IgG, IgA or IgE) without changing its specificity for antigen, this phenomenon is
called class switching, or isotype switching;
2.Genetic foundation: It results from a specialized type of DNA rearrangement between a same V-region gene with
different C-region genes;
3.Charateristic: occurs on antigen stimulation; strongly influenced by cytokines produced by Th cells.
 Formation of plasma cells
1.Synthesize and secrete specific Ab;
2.Most transfer to bone marrow and generate Ab continuously;
3.Don’t express BCR and MHC class Ⅱ molecule, can’t react to Ag and lose the ability to react with Th.
 Generation of Memory B cells (Bm)
1.Most of memory B cells enter blood and participate recirculation;
2.Have a higher affinity receptor and more readily activated to proliferate and secrete antibody by antigen
stimulation in secondary response ;

Chapter 2 B Cell Response to TI-Ag

B cell response to TI-1 antigens
 At high concentration: TI-1 Ag acts with B cell as a mitogen;
 At low concentrations: TI-1 Ag elicits an antigen-specific antibody response.
B cell response to TI-2 antigens
 TI-2 antigens are generally highly repetitive polymeric antigens.
 TI-2 antigens activate B cells through cross-linking of BCR molecules
Characteristics of B cell response to TI-Ag
 Don’t require the presence of Th cells;
 No somatic hypermutation, no affinity maturation, no Ig heavy-chain class switching and no Bm formation;
 Generates primarily IgM antibodies of low affinity.

Chapter 3 Rules of Antibody Production

Primary response
 Most of the antigens are processed by dentritic cells;;
 Develop in 5-10 days after antigen introduction, 15-20 days required to reach peak serum antibody concentration;
 Achieve low antibody concentration;
 Duration is short;
 The antibodies initially produced are predominantly IgM with low antigen affinities.
Secondary response
 Meromy B cells serves as the principal APCs;
 Shorter lag peroid;
 Activated at very low concentrations of antigen;
 Achieve high affinity and high concentration of antibody;
 Duration is long;
 IgG tends to predominate.

Chapter 4 Effects of B cell Mediated Humoral Immune Response

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Effects of antibody
 neutralization
 complement activation
 opsonization
 ADCC
 participate typeⅠhypersensitivity
 cross the placenta and mucosa

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Section 14 Inate Immune system and Innate Immune Response

Chapter 1 Components of Innate Immune System

Tissue barriers;
 The skin and the mucosal surfaces
1. Physical barrier: prevent microorganisms and other potentially injurious agents from entering the tissues beneath.
2. Chemical barrier: secrete substances that can kill or inhibit pathogens.
3. Microbiological barrier: normal flora
 Barriers in vivo
1. blood-brain barrier: prevent pathogens from entering brain tissues
2. blood-embryo barrier: prevent pathogens of mother from entering fetus
Innate immune cells;
phagocyte(monocyte/macrophage, neutrophil), dendritic cell(DC), natural killer cell(NK cell), Innate-like lymphocyte
(ILL)NKT Cell, gdT cell, B1 cell
 Pattern recognition receptor (PRR): PRRs refer to the receptors expressed on multiple types of immue cells including
phagocytes and dendritic cells and on the membrane of intracellular organelles and in the serum, which can directly
recognize some certain molecular structures that owned by pathogens and their products, and apoptotic, aging or
impaired body cells.
 Pathogen associated molecular pattern (PAMP): PAMPs refer to the highly conserved certain molecular structures
that owned by some pathogens and their products, and apoptotic, aging or impaired body cells and can be recognized
by pattern recognition receptors (PRR).
 Macrophage
Major biological functions of macrophages
1) Kill and clear pathogens;
2) Kill target cells;
3) Participate inflammation;
4) Process and present antigens to initiate adaptive immune response;
5) Immunological regulation.
 Natural killer cell (NK cell)
1. Distribution: bone marrow, peripheral blood, liver, spleen, lungs and lymph nodes.
2. Surface markers: TCR-, mIg-, CD56+, CD16+
3. Functions: anti-infection, anti-tumor, Immunological regulation.
4. Characteristics: Directly kill tumor cells and virus-infected cells without the need for prior immunization; act as an
effector in ADCC.
5. Killing mechanisms: Perforin/granzymes pathway, Fas/FasL pathway, TNF-a/TNFR pathway.
6. Modulation of NK cells activity( Mechanisms of NK cells to recognize “self” and “non-self”)
1) Under physiological conditions, the inhibitory receptors (KIR2DL/3DL and CD94/NKG2A) play a dominant
role. They recognize MHC classⅠmolecules expressed on self tissue cells and inhibit the the function of the
activating receptors. So NK cells can not kill self normal tissue cells.
2) Under pathological conditions, surface MHC classⅠ molecules expressed on tumor cells and virus-infected cells
are decreased or lost, so the inhibitory receptors have no ligands and lose negative regulatory activity. At the
same time, the activating receptors (NCR and NKG2D) recognize non-MHC classⅠmolecules which abnormally
or increasedly expressed on tumor cells and virus-infected cells, and induce killing activity of NK cells to kill

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the target cells.

Innate Immune Molecules
 Complement system;
 Cytokines;
 Other antibacterial substances: antibacterial peptide, lysozyme, b-lysin.

Chapter 2 Innate Immune Response and the Relationship Between Innate and Adaptive Immune Response

Three phases of innate immune response

 Immediate innate immunity stage (0-4 hours);
 Early induced innate immune response stage (4-96 hours);
 Adaptive immune response initiated stage (after 96 hours)..
The relationship between innate and adaptive immune response
 Initiate adaptive immune response;
 Regulate the type and intensity of adaptive immune response;
 Innate immunity activates adaptive immunity;
 Help effector T cells to entering the position where infection or tumor take place;
 Assist effetor T cells and antibodies to exert immune effects.

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Section 15 Immunological Tolerance

Definition: Immunological tolerance is a state of unresponsiveness that is specific for a particular antigen.

Chapter 1 The Development of Immunological Tolerance

Immunological tolerance induced in embryonic stage and newborn Stage

Immunological tolerance induced by Ag after birth
 Antigenic factors
1. Antigen dosage: low-zone tolerance, high-zone tolerance;
2. Type of antigen;
3. Route of Ag Immunization;
4. Antigen persistence;
5. Characteristics of epitope
 Organic factors
1. Age and developmental stage;
2. Physiological status
3. Genetic background

Chapter 2 Mechanisms of Immunological Tolerance

Central tolerance: refers to the tolerance that is induced in central immune organs as a consequence of immature self-
reactive lymphocyte recognizing self-antigen
Peripheral tolerance refers to the tolerance that is induced in peripheral sites as a result of mature lymphocyte
encountering endogenous or exogenous antigen under particular conditions
 Clonal deletion
 Immunological ignorance;
 Clonal anergy;
 Functions of immunological regulatory cells;
 Antigens in immunological privileged sites do not induce immune response under physiological conditions.

Chapter 3 Immune Tolerance and Clinical Medicine

Induction of immunological tolerance

Abrogation of immune tolerance

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Section 17 Hypersensitivity
Definition ： The abnormal adaptive immune responses to some antigens which result in disorders of physiological
functions or damage of tissue cells are called hypersensitivity.

Classification
Four types of hypersensitivity: typeⅠ,Ⅱ, Ⅲ, Ⅳ.
 TypeⅠ,Ⅱ, Ⅲ are antibody-mediated (humoral immunity), type Ⅳ is T cell mediated (cellular immuntiy).
 TypeⅠ: allergy, anaphylaxis, immediate hypersensitivity.
 TypeⅡ: cytotoxic type.
 TypeⅢ: immune complex type.
 TypeⅣ: delayed type.

Chapter 1 TypeⅠHypersensitivity
Major features
 TypeⅠhypersensitivity is a IgE-mediated localized or systemic response which is induced by the bioactive mediators
released by mast cells and basophils;
 React and disappear quickly;
 Cause dysfunction rather than severe tissue and cell damage;
 Have obvious individual difference and genetic correlation
 Have obvious individual difference and genetic correlation
Component and cells
 Allergens;
 IgE and IgE-binding Fc receptors;
1. IL-4 produced by Th2 cell results in the production of IgE;
2. Two classes of FcεR: FcεRⅠ, FcεRⅡ;
FcεRⅠ: the high affinity receptor, highly expressed on mast cell and basophil;
FcεRⅡ: the low affinity receptor.
 Mast cells, basophils and eosinophils.
Mechanisms of TypeⅠHypersensitivity
 Sensitization
 IgE receptor crosslinking and cell activation
 Bioactive mediators release
1. Classified as either primary or secondary.
2. Primary mediators: stored in the granules, such as histamine, kininogenase..
3. Secondary mediators: newly synthesized, such as platelet activating factor(PAF), leukotrienes(LTs), prostaglandin
D2(PGD2), and cytokines.
4. Effectors: contraction of smooth muscle, dilatation of capillaries, increase of permeability, gland hypersecretion.
 Systemic and localized anaphylaxis
1. Immediate reaction
2. Late-phase reaction

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The Mechanism of TypeⅠ Hypersensitivity

first generation
allergen body I gE
adsorption
subsequent I gE binds the Fcε RⅠ on the surface of mast cell and basophil

allergen binds to I gE specificly on the surface of sensitized target cell

Fcε RⅠ cross- linking
degranulation of mast cell and release of bioactive mediators

kininogenase histamine PGD2 LTs PAF cytokines

contraction of smooth muscle, dilatation of capillaries, increase

of permeability, gland hypersecretion

systemic skin respiratory tract digestive tract

(anaphylactic shock) (urticaria) (allergic rhinitis, (anaphylactic gastroenteritis)
asthma)

TypeⅠhypersensitivity-associated diseases
 Systemic anaphylaxis: anaphylactic shock;
 Localized anaphylaxis: allergic rhinitis and asthma, anaphylactic gastroenteritis, urticaria, atopic
dermatitis(eczema).
Therapy for typeⅠhypersensitivity
 Identification of the offending allergen and avoiding contact: skin test.
 Hyposensitization: immunotherapy with repeated injections of small dose of allergens to reduce the severity of
typeⅠreactions, or even eliminate them completely.
 Drugs.
 Immunobiotherapy.

Chapter 2 TypeⅡHypersensitivity

Summary
 Mediated by IgG and IgM;
 Antibodys bind to the antigens on target cell surfaces;
 Under the participation of complements, phagocytes and NK cells;
 Cause cell lysis or tissue damage-based pathologic immune response.
Mechanisms of TypeⅡHypersensitivity
TypeⅡhypersensitivity-associated diseases
 Transfusion reaction;
 Hemolytic disease of the newborn;
 Autoimmune hemolytic anemia;
 Drug allergic cytopenia;

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 Goodpasture syndrome
 Grave’s disease and myasthenia gravis.

The mechanism of TypeⅡ hypersensitivity

Antigen on the surface of the cell or

antigen, hapten adsorbed on the surface of the cell
+
Specific antibody (I gG, I gM)

Complement activation Opsonization NK cell, phagocyte Stimulation or block

Lysis of target cell Phagocytose of target cell ADCC

Target cell
dysfunction
Target cell damage

Chapter 3 TypeⅢHypersensitivity
Summary
 Mediated by medium-sized soluble immune complexes deposition;
 Complexes deposit on the capillary basement membrane and induce inflammatory reaction and tissue damage
characterized by edema, local necrosis and neutrophil infiltration via complement activation and under the
participation of neutrophils, platelets and basophils.
Mechanisms of type Ⅲ hypersensitivity
Type Ⅲ hypersensitivity-associated diseases
 Localized type Ⅲ reaction: Arthus reaction;
 Systemic type Ⅲ reaction: serum sickness; post-streptococcal glomerulonephritis; rheumatoid arthritis; systemic
lupus erythematosus(SLE).a

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Stimulate Generate
Soluble Ag Body Ab( I gG, I gM, I gA)

I mmune complex
Engulfed by phagocytes
Deposit on capillary basement membrane or cleared through
glomcrulus
Complement activation
Basophils and platelets
mast cells C3a,C5a,C3b
blood clotting Release vasoactive
Release vasoactive Nuetrophils system substances
substances infiltration
interspace of vascular interspace of
Engulf immune aggregation
endothelial cells vascular endothelial
complex of platelets
increase cells increase
microthrombus
Vasopermeability Release Vasopermeability
formation
enhance lysosomal enzyme enhance
ischemia
edema Tissue damage edema
bleeding

Localized or systemic immune complexes disease

Chapter 4 Type Ⅳ Hypersensitivity

Summary
 Mediated by effector T cells;
 Effector T cells bind to specific antigens and induce inflammatory reaction characterized by mononuclearcells
infiltration and tissue lesion;
 Occurs in 24-72 hours after contacting with the same antigen (delayed type hypersensitivity, DTH);
 Has nothing to do with antibody and complement
mechanisms of Type Ⅳ hypersensitivity
Type Ⅳ hypersensitivity-associated diseases
 Infectious DTH: tuberculosis;
 Contact DTH: contact dermatitis.
 Th2 mediated DTH: chronic asthma

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Macrophage
induce infiltration
Cytokine
Antigen T cell I L- 2 T cell
(CD4+,CD8+) I FN- r proliferation
TNF- β
CD4+ Exudation
MCF inflammatory
T cell reaction
MI F cytotoxicity characterized by
mononuclearcells
infiltration and
tissue lesion

Re- exposure
Sensitized T cell
(CD4+,CD8+)

CD8+ Killing target

T cell cell

The Mechanism of Type Ⅳ Hypersensitivity

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Section 18 Autoimmune Diseases

Definition:
 Autoimmunity refers to the immune response against self antigens, which helps to eliminate the aging or denatured
self components and to maintain the immune homeostasis in the condition of immunological tolerance.
 Autoimmune diseases refer to the clinical diseases result from abnormal immune responses against self antigens
which cause selft cells and tissues damage or dysfunction in the condition of immunological tolerance breaking.

Chapter 1 Factors and Mechanisms in Development of Autoimmune Diseases

Factors in development of autoimmune diseases

 Antigenic factors
1.Release of antigens in immunologically privileged sites: sympathetic ophthalmia;
2.Alteration of self antigens
3.Molecular mimicry: Some pathogens express antigens that resemble host molecules. In such cases, immune
responses react against the foreign antigen, and also cross-react with self antigens. This form of tolerance breaking
is called molecular mimicry.
4.Epitope spreading: The immune system usually response firstly against the dominant epitope of an antigen. The
immune responses induced may injury tissues and result in the release and exposure of the cryptic epitopes which
can activate lymphocytes specific for these epitopes and exacerbate the disease. This phenomenon is called epitope
spreading.
 Genetic factors
1.MHC genes have the strongest association with autoimmune diseases.
2.Other genes associated with autoimmune diseases.
 Other factors
1.Gender factors
2.Age factors
3.Enviromental factors
Mechnisms of immunological tolerance abnormality
 Abnormality of autoreactive lymphocytes clearance;
 Immunological ignorance breaking;
 Polyclonal activation of lymphocytes;
 Disorder of activation-induced cell death;
 Dysfunction of regulatory T cells;
 Abnormality of MHC classⅡmolecules expression.

Chapter 2 Pathological Damage Mechanisms of Autoimmune Diseases

Autoantibodies mediated autoimmune diseases

 Autoantibodies directly mediate cell damage
1. Mechanisms: TypeⅡhypersensitivity
2. Typical diseases:
(1)Autoimmune cytopenia: autoimmune anemia, autoimmune thrombocytopenic purpura, autoimmune neutropenia.
(2)Pernicious anemia
 Autoantibodies mediate cell dysfunction

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1. Mechanisms: Special typeⅡhypersensitivity

2. Typical diseases:
(1)Graves disease : stimulate the function
(2)Myasthenia gravis (MG): block the function
 Autoantibodies form immune complexes with self antigens to mediate tissue damage
1. Mechanisms: Type Ⅲ hypersensitivity
2. Typical diseases:
(1)Systemic lupus erythematosus (SLE)
(2)Rheumatoid arthritis (RA)
Autoreactive T cells mediated autoimmune disease
 Mechanisms: Type Ⅳ hypersensitivity
 Typical diseases
1. Insulin-dependent diabetes mellitus (IDDM)
2. multiple sclerosis (MS)

Chapter 3 Classification and Characterisitcs of Autoimmune Diseases

Classification
 Organ specific autoimmune disease: Graves’ disease, IDDM；
 Systemic autoimmune disease: SLE, RA

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Section 19 Immunodeficiency Diseases

Definition: Immunodeficiency disease (IDD) refers to the clinical syndrom which is characterized by loss of immune
components and disorder of immune function caused by congenital hypoplasia or postnatal damage of immune system.
Classification
 Primary immunodeficiency disease(PIDD)/Congenital immunodeficiency disease(CIDD)
 Acquired immunodeficiency disease(AIDD)

Chapter 1 Primary Immunodeficiency Diseases

Definition: PIDD are diseases of immunologic inadequacy caused by genetic genes abnormality or congenital
hypoplasia of immune system.
Combined B cell and T cell immunodeficiencies
 SCID(severe combined immunodeficiency disease, SCID) is characterized by developmental disorder of T cells and
B cells or lack of interaction between cells.
 T-B+SCID, T-B-SCID
Antibody immunodeficiencies
 Antibody immunodeficiency is characterized by defect of antibody generation and function, usually with decrease or
lack of serum Ig.
 X-linked agammaglobulinaemia(XLA), common variable immunodeficiency(CVID)
Phagocytic defects
 Phagocytic defects are characterized by disorders of chemotaxis, adhesion ability and bactericidal activity of
phagocytes.
 Chronic granulomatous disease(CGD)
Complement deficiencies
 In complement system, the complement innate components, the complement regulatory proteins and the complement
receptors all can be deficient.
 Hereditary angioneurotic edema (C1INH deficiency), paroxysmal nocturnal hemoglobinuria(PNH, dificiency of DAF
and MIRL).
Other well defined immunodeficiency syndromes
 Wiskott-Aldrich syndrome(WAS)

Chapter 2 Acquired Immunodeficiency Diseases

Factors inducing AIDD

 Non-infection factors
malnutrition, malignant tumor, immunosuppressive drugs, radiographic exposure, etc.
 Infection
HIV(human immunodeficiency virus), EB virus, etc.
Acquired immunodeficiency syndrome(AIDS)
AIDS is the disease caused by infection with HIV and is characterized by profound immunosuppression with
associated opportunistic infections, malignant tumors and central nervous system degeneration.

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Section 20 Tumor Immunology

Chapter 1 Tumor Antigens

Definition: Tumor antigens refer to the neoantigens appeared during cells canceration and the antigenic substances
abnormally expressed or overexpressed by tumor cells.
Classification and characteristics of tumor antigens
 Classification by specificity of tumor antigen
 Classification by specificity of antigen
1. Tumor specific antigen(TSA)
1)Definition: Tumor specific antigens are neoantigens can be detected only in tumor cells and not in other host
cells
2)Tumor specific transplantation antigen(TSTA) or tumor rejection antigen(TRA).
2.Tumor-associated antigen(TAA)
Definition: Tumor-associated antigens are found in tumor cells and also in some normal cells, but their quantity
increase obviously during cancerization and permit the use of these antigens to distinguish tumor cells from normal
cells
 Classification by generation mechanism of tumor antigen
1.Products of mutant genes or oncogenes
2.Abnormally expressed cell proteins
3.Tumor antigens expressed by oncogenic virus
4.Fetal antigen
5.Tissue specific differentiation antigen
6.Abnormal cell proteins and their products resulted from glycosylation

Chapter 2 Mechanisms of Anti-Tumor Effects

Characteristics of the immune response against tumor

 Immunological function is closely related to the genesis and development of tumor;
 Innate immune response and adaptive immune response both play role in anti-tumor response
 Innate immunity is the first line against tummor；
 Cellular immunity is the main force in anti-tumor immunity (CD8+CTL and CD4+Th), humoral immunity have
synergistic effects.

Chapter 3 Mechanisms of Tumor Escape

 Capabilities of tumors to escape immune surveillance

 Antigenic deletion and antigenic modulation;
 Low expression of MHC classⅠmolecules;
 Abnormality of costimulatory signals;
 Express or secrete immunosuppressive molecules；
 Resistant to apoptosis；
 Induce apoptosis of tumor specific T cells and inhibit activation and proliferation of T cells；
 Induce the generation of Tregs and myeloid-derived suppressor cells(MDSCs).
 Functions of tumor microenvironments

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 Influences of host immune function

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Section 21 Transplantation Immunology

Definition: Transplantation refers to the act of transferring cells, tissues, or organs (a graft) between individuals of same
or different species.
Classification of transplantation
 Autologous transplantation
 Syngeneic transplantation
 Allogeneic transplantation
 xenogeneic transplantation

Chapter 1 Mechanism of Allograft Rejection

Target antigens of allograft rejection

 Major histocompatibility antigens(MHC)
 Minor histocompatibility antigens
 Other target antigens in allograft rejection: human ABO blood group antigen; tissue specific antigen .
Mechanisms in alloantigen recognition of T cells
 Direct recognition
1. Alloreactive T cells of recipient directly recognize peptide-donor’s MHC complex on donor’s APC surface and
generate immune response.
2. The principal mechanism in the early period of acute rejection.
 Indirect reconition
1. Cast-off cells from the donor’s graft are captured and processed by recipient’s APC to form donor’s peptide-
recipient’s MHC complexes which are presented to recipient’s T cells for recognition and activation.
2. The principal mechanism in the middle and late period of acute rejection and chronic rejection.
Effect mechanisms of graft rejective reaction
 Effects of cellular immune response
 Effects of humoral immune response
 Effects of innate immune response

Chapter 2 Allograft rejection types

Host versus graft reaction (HVGR)

 Definition: After transplantation, recipient’s immune system recognize graft antigen and generate immune response
to reject the graft.
 Classification:
1. Hyperacute rejection
(1) Definition: the rejection occurs in several minutes to 24 hours after the blood vessels between transplanted organ
and recipient are connected. It is seen in repeated transfusion, multiple pregnancy, long-term hemodialysis and
retransplantation individuals.
(2) Mechanisms: There are antibodies against donor’s tissue antigens pre-exist in recipient.
2. Acute rejection
(1) Definition: It is the most frequent rejection in allogeneic organ transplantation. It occurs in several days to 2 weeks

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after transplantation.
(2) Mechanism: cellular immune responses play major roles.
3. Chronic rejection
(1) It occurs in several weeks, or several months even several years after transplantation.
(2) Mechanism: 1)Immunological mechanism: chronic vascular rejection(VCR), which is characterized by damage of
blood vessel endothelium in transplanted organs. 2) Non-immunological mechanism: degeneration of the organ.
Graft versus host reaction(GVHR)
 Definition: The antigen-specific lymphocytes in graft recognize the recipient’s tissue antigens and generate immune
response to induce rejection.

Section 23 Immunoprophylaxis and Immunotherapy

Chapter 1 Immunoprophylaxis

Artificial immunization
 Artificial active immunization: Vaccines are inoculated in order to generate adaptive immune response actively, thus
prevent or treat diseases.
 Artificial passive immunization: The preparations contain specific antibodies such as antitoxin are injected to let the
body to acquire adaptive immune response passively, in order to treat or prevent disease in emergency
Vaccine
 Definition: The biological agents which can induce specific immunity against certain diseases after inoculation are
collectively called vaccines.
Basic requirements of vaccines
 Security
 Valid
 Practical
Types of vaccines
 Inactivated vaccine
 Live-attenuated vaccine
 Toxoid
 Subunit vaccine
 Conjugate vaccine
 DNA vaccine
 Recombinant vector vaccine

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英中文索引
Section 1

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immunity 免疫 immune defense 免疫防御

im antigen, Ag 抗原 immune surveillance 免疫监视
mune system 免疫系统 immune homeostasis 免疫自身稳定
immune organ 免疫器官 physiological 生理的
central immune organ 中枢免疫器官 pathological 病理的
peripheral immune organ 外周免疫器官 hypersensitivity 超敏反应
bone marrow 骨髓 immunodeficiency disease 免疫缺陷病
thymus 胸腺 immunological tolerance 免疫耐受
lymph node 淋巴结 immunological regulation 免疫调节
spleen 脾 autoimmune disease 自身免疫性疾病
phagocyte 吞噬细胞 immune response 免疫应答
lymphocyte 淋巴细胞 innate immunity 固有免疫
dendritic cells，DC 树突状细胞 adaptive immunity 适应性免疫
T cell receptor，TCR T 细胞（抗原）受体 acquired immunity 获得性免疫
B cell receptor，BCR B 细胞（抗原）受体 humoral immunity 体液免疫
cluster of differentiation，CD （抗原）分化群 cellular immunity 细胞免疫
adhesion molecule，AM 黏附分子 antigen-presenting cell, APC 抗原提呈细胞
antibody，Ab 抗体 effector T cell 效应 T 细胞
complement，C 补体 helper T cell, Th 辅助 T 细胞
cytokine，CK 细胞因子 clonal selection theory 克隆选择学说
mucosal-associated lymphoid tissue，MALT 黏膜相关淋巴组织
major histocopatibility complex，MHC 主要组织相容性复合体

Section 2

1
immune tissue 免疫组织 alimentary tract 消化道
primary lymphoid organ 初级淋巴器官 genitourinary tract 泌尿生殖道
secondary lymphoid organ 次级淋巴器官 respiratory tract 呼吸道
hematopoiesis 造血 tonsil 扁桃体
hematopoietic inductive microenvironment, HIM 造血微环境 Peyer’s patches 派氏集合淋巴结
hematopoietic stem cell, HSC 造血干细胞 appendix 阑尾
secondary humoral immunity 再次体液免疫 secretory IgA，SIgA 分泌型 IgA
thymic stromal cell, TSC 胸腺基质细胞 lymphocyte homing 淋巴细胞归巢
extracelluar matrix 细胞外基质 homing receptor 归巢受体
thymic microenvironment 胸腺微环境 vascular addressin 血管地址素
self tolerance 自身耐受 lymphocyte recirculation 淋巴细胞再循环
epithelia 上皮
Section 3
immunogenicity 免疫原性 adjuvant 佐剂
Immunoreactivity 免疫反应性 thymus dependent antigen，TD-Ag 胸腺依赖性抗原
immunogen 免疫原 thymus independent antigen，TI-Ag 胸腺非依赖性抗原
complete antigen 完全抗原 heterophilic antigen 异嗜性抗原
hapten 半抗原 hemolytic streptococcus 溶血性链球菌
incomplete antigen 不完全抗原 xenogenic antigen 异种抗原
epitope （抗原）表位 allogenic antigen 同种异型抗原
antigenic determinant 抗原决定簇 human leukocyte antigen，HLA 人类白细胞抗原
sequential epitope 顺序表位 autoantigen 自身抗原
conformational epitope 构象表位 idiotypic antigen 独特型抗原
antigenic valence 抗原结合价 endogenous antigen 内源性抗原
common epitope 共同（抗原）表位 exogenous antigen 外源性抗原
common antigen 共同抗原 phagocytosis 吞噬
cross-reaction 交叉反应 endocytosis 胞吞
foreignness 异物性 pinocytosis 胞饮
conformation （分子）构象 superantigen，SAg 超抗原
accessibility 易接近性 mitogen 丝裂原
Section 4
Immunoglobulin, Ig 免疫球蛋白 in vivo 体内
plasma cell 浆细胞 in vitro 体外
serum 血清 neutralize 中和
membrane Ig，mIg 膜型 Ig toxin 毒素
heave chain 重链 immunodiagnosis 免疫诊断
light chain 轻链 classical pathway 经典途径
disulfide bond 二硫键 alternative pathway 旁路途径
domain 结构域 opsonization 调理作用
variable region 可变区 macrophages 巨噬细胞
constant region 恒定区 neutrophil 中性粒细胞
hypervariable region，HVR 高变区 mast cell 肥大细胞
framework region，FR 骨架区 basophil 嗜碱性粒细胞
complementarity-determining regions，CDR 互补决定区 cross-link 交联
hinge region 铰链区 placenta 胎盘
flexibility 弹性，柔性 monomer 单体
protease 蛋白酶 dimer 二聚体
joining chain J 链 macroglobulin 巨球蛋白
secretory piece，SP 分泌片 pentamer 五聚体
papain 木瓜蛋白酶 molecular weight 分子量
pepsin 胃蛋白酶 secondary immune response 再次免疫应答
fragment of antigen binding，Fab 抗原结合片段 differentiation 分化
fragment crystallizable，Fc 可结晶片段 affinity 亲和力
monovalent 单价的 polyclonal antibody，pAb 多克隆抗体
bivalent 二价的 monoclonal antibody，mAb 单克隆抗体
isotype 同种型 homogeneous 同质的，同种的
allotype 同种异型 hybridoma 杂交瘤
idiotype 独特型 genetic engineering antibody 基因工程抗体
antibody-dependent cell-mediated cytotoxicity，ADCC 抗体依赖的细胞介导的细胞毒作用
Section 5
enzymatic cascade reaction 酶促级联反应 lipopolysaccharide，LPS 脂多糖
zymogen 酶原 zymosan 酵母多糖
inflammation 炎症 polyglucosan 葡聚糖
mannose-binding lectin，MBL 甘露糖结合的凝集素 ficolin, FCN, 纤维胶原素
properdin 备解素 carbohydrate 糖，碳水化合物
C1 inhibitor，C1INH C1 抑制物 membrane attack complex，MAC 攻膜复合物
C4 binding protein，C4bp C4 结合蛋白 immune adherence 免疫黏附
complement regulatory protein 补体调节蛋白 erythrocyte 红细胞
complement receptor，CR 补体受体 platelet 血小板
decay accelerating factor，DAF 衰变加速因子 anaphylatoxin 过敏毒素
membrane cofactor protein，MCP 膜辅助蛋白 degranulation 脱颗粒
S protein，SP S 蛋白 bioactive substance 生物活性物质
C8 binding protein，C8bp C8 结合蛋白 chemotaxis 趋化作用
immune complex,，IC 免疫复合物 migration 迁移
C3 convertase C3 转化酶 pathophysiological 病理生理的
C5 convertase C5 转化酶 cascade reaction 级联反应
MBL associated serine protease，MASP MBL 相关的丝氨酸蛋白酶

Section 6
peptide 肽 hemorrhagic necrosis 出血性坏死
glycoprotein 糖蛋白 cachectin 恶液质素
autocrine action 自分泌作用 lymphotoxin，LT 淋巴毒素
paracrine action 旁分泌作用 apoptosis 凋亡
endocrine action 内分泌作用 colony-stimulating factor，CSF 集落刺激因子
pleiotropism 多效性 pluripotent stem cell 多能干细胞
redundancy 重叠性 progenitor 前体
antagonism 拮抗性 granulocyte 粒细胞
synergy 协同性 stem cell factor，SCF 干细胞因子
Interleukin，IL 白细胞介素 erythropoietin，EPO 红细胞生成素
Interferon，IFN 干扰素 thrombopoietin，TPO 血小板生成素
leukocyte 白细胞 chemokine 趋化因子
fibroblast 成纤维细胞 growth factor，GF 生长因子
natural killer，NK 自然杀伤细胞 epidermal growth factor，EGF 表皮生长因子
tumor necrosis factor，TNF 肿瘤坏死因子 fibroblast growth factor，FGF 成纤维细胞生长因子
transforming growth factor-β，TGF-β 转化生长因子 -β
vascular endothelial growth factor，VEGF 血管内皮细胞生长因子

Section 7
leukocyte differentiation antigen 白细胞分化抗原 integrin family 整合素家族
lineage 谱系 selectin family 选择素家族
nomenclature 命名 immunoglobulin superfamily，IgSF 免疫球蛋白超家族
cell adhesion molecule，CAM 细胞黏附分子 cadherin family 钙粘蛋白家族
extracellular matrix 细胞外基质 vascular endothelial cell 血管内皮细胞
ligand 配体

Section 8
major histocompatibility antigen 主要组织相容性抗原 thymic epithelial cells 胸腺上皮细胞
MHC antigen/MHC molecule MHC 抗原/MHC 分子 codominance 共显性
human leukocyte antigen, HLA 人类白细胞抗原 endogenous antigenic peptide 内源性抗原肽
HLA gene complex HLA 基因复合体 exogenous antigenic peptide 外源性抗原肽
HLA antigen/HLA molecule HLA 分子/HLA 抗原 peptide-binding groove 抗原肽结合槽
polygenism 多基因性 anchor positions 锚定位
chromosome 染色体 anchor residue 锚定残基
HLA(MHC) classⅠmolecule HLA(MHC)Ⅰ 类分子 consensus motif 共用基序
HLA(MHC) classⅡmolecule HLA(MHC)Ⅱ 类分子 MHC restriction MHC 限制性
β2 microglobulin，β2m β2 微球蛋白 graft rejection 移植排斥
polymorphism 多态性 disease susceptibility 疾病易感性
linkage disequilibrium 连锁不平衡 inflammatory reaction 炎症反应
haplotype 单体型 stress reaction 应激反应
antigen-presenting cell，APC 抗原提呈细胞
Major histocompatibility complex, MHC 主要组织相容性复合体

Section 9
germline gene 胚系基因 pre-B cell 前 B 细胞
rearrangement 重排 immature B cell 未成熟 B 细胞
recombinase 重组酶 mature B cell 成熟 B 细胞
recombination signal sequence RSS 重组信号序列 central tolerance 中枢（免疫）耐受
allelic exclusion 等位排斥 negative selection 阴性选择
isotypic exclusion 同型排斥 clone deletion 克隆清除
combinational diversity 组合多样性 anergy 无能
junctional diversity 连接多样性 heterodimer 异源二聚体
receptor editing 受体编辑 coreceptor 共受体
somatic hypermutation 体细胞高频突变 co-stimulatory molecule 共刺激分子
pro-B cell 祖 B 细胞 subset 亚群
immunoreceptor tyrosine-based activation motif，ITAM 免疫受体酪氨酸激活基序
immunoreceptor tyrosine-based inhibition motif，ITIM 免疫受体酪氨酸抑制基序

Section 10
ontogeny 个体发育 memory T cell，Tm 记忆 T 细胞
thymic cortex 胸腺皮质 helper T cell，Th 辅助 T 细胞
thymic medulla 胸腺髓质 cytotoxic T cell，CTL/Tc 细胞毒性 T 细胞
cortico-medullary junction 皮髓质交界处 regulatory T cell，Treg 调节性 T 细胞
double positive cell，DP 双阳性细胞 class switching 类别转换
double negative cell，DN 双阴性细胞 eosinophil 嗜酸性粒细胞
single positive cell，SP 单阳性细胞 microorganism 微生物
positive selection 阳性选择 perforin 穿孔素
negative selection 阴性选择 granzyme 颗粒酶
heterodimer 异二聚体 granulysin 颗粒溶素
homodimer 同源二聚体 polymerize 聚合
naïve T cell 初始 T 细胞 osmotic swelling 渗透膨胀
effector T cell 效应 T 细胞 caspase 胱天蛋白酶
cytotoxic T lymphocyte antigen-4，CTLA-4 细胞毒性 T 淋巴细胞抗原-4

Section 11
antigen-presenting cells, APC 抗原提呈细胞 follicular DC，FDC 滤泡样 DC
antigen presentation 抗原提呈 interstitial DC 间质性 DC
antigen processing 抗原加工或抗原处理 Langerhans cell，LC 朗格汉斯细胞
professional APC 专职性 APC veiled cell 隐蔽细胞
non-professional APC 非专职性 APC monocyte 单核细胞
conventional DC (cDC) 经典 DC macrophage 巨噬细胞
plasmacytoid DC (pDC): 浆细胞样 DC exogenous antigen 外源性抗原
myeloid DC 髓系 DC endogenous antigen 内源性抗原
lymphoid DC 淋巴系 DC ubiquitin 泛素
interdigitating DC，IDC 并指状 DC ubiquitinated 泛素化的
proteasome 蛋白酶体 merge 融合
cytoplasm 细胞浆（细胞质） endosome 内体
rough endoplasmic reticulum，RER 粗面内质网 phagosome 吞噬体
lumen 腔 lysosome 溶酶体
chaperone 伴侣蛋白 phagolysosome 吞噬溶酶体
calnexin 钙联蛋白 nonamer 九聚体
tapasin TAP 相关蛋白 assemble 组装
subunit 亚单位 fole 折叠
assemblage 集合体 Ia-associated invariant chain，Ii Ia 相关恒定链
low molecular weight peptide, LMP 低分子量多肽 MHC classⅡcompartment，MⅡC MHCⅡ 类分子腔室
cytosolic 细胞溶质的
proteasome subunit beta type, PSMB 蛋白酶体 b 亚单位
transporter associated with antigen processing，TAP 抗原加工相关转运物
classⅡ-associated invariant chain peptide，CLIP MHCⅡ 类分子相关的恒定链多肽

Section 12
intercellular adhesion molecule，ICAM 细胞间黏附分子 recruit 招募
immunological synapse 免疫突触 polarization 极化
signals transduction 信号转导 lethal hit 致死性攻击
outcome 转归 phenotype 表型
lymphocyte function associated antigen，LFA 淋巴细胞功能相关抗原
activation-induced cell death, AICD 活化诱导的细胞死亡

Section 13
germinal center 生发中心 Ig class switching Ig 类别转换
dark zone 暗区 isotype switching 同种型转换
light zone 明区 memory B cell，Bm 记忆性 B 细胞
centroblast 中心母细胞 lymphoid follicle 淋巴滤泡
centrocyte 中心细胞 lag peroid 潜伏期
somatic hypermutation 体细胞高频突变 primary response 初次应答
point mutation 点突变 secondary response
affinity maturation 亲和力成熟

Section 14
tissue barriers 组织屏障 pattern recognition receptors，PRRs 模式识别受体
microbiological 微生物的 organelle 细胞器
normal flora 正常菌群 peripheral blood 外周血
blood-brain barrier 血脑屏障 antibacterial peptide 抗菌肽
blood-embryo barrier 血胎屏障 lysozyme 溶菌酶
fetus 胎儿 β-lysin 乙型溶素
innate-like lymphocyte, ILL 固有样淋巴细胞
killer lectin-like receptor，KLR 杀伤细胞凝集素样受体
natural cytotoxicity receptors，NCR 自然细胞毒性受体
killer immunoglobulin-like receptor，KIR 杀伤细胞免疫球蛋白样受体
pathogen associated molecular patterns，PAMPs 病原相关分子模式

Section 15
immunological tolerance 免疫耐受 tolerogenic epitope 耐受原表位
unresponsiveness 免疫无应答 central tolerance 中枢耐受
tolerogen 耐受原 peripheral tolerance 外周耐受
embryonic Stage 胚胎期 clonal deletion 克隆清除
newborn stage 新生期 immunological ignorance 免疫忽视
low-zone tolerance 低带耐受 clonal anergy 克隆失能
high-zone tolerance 高带耐受 immunological privileged sites 免疫豁免部位
split tolerance 耐受分离

Section 17
Hypersensitivity 超敏反应 asthma 哮喘
allergy 变态反应 digestive tract 消化道
anaphylaxis 过敏反应 gastroenteritis 胃肠炎
immediate hypersensitivity 速发型超敏反应 immediate reaction 速发相反应
cytotoxic type 细胞毒型 late phase reaction 迟发相反应
immune complex type 免疫复合物型 recruitment 募集
delayed type 迟发型 atopic dermatitis 特应性皮炎
dysfunction 功能障碍 eczema 湿疹
bioactive mediators 生物活性介质 skin test 皮肤试验
individual difference 个体差异 hyposensitization 脱敏
genetic correlation 遗传相关 Immunobiotherapy 免疫生物疗法
allergen 变应原 transfusion reaction 输血反应
sensitization 致敏作用 hemolytic disease of the newborn 新生儿溶血症
crosslinking 交联 Autoimmune hemolytic anemia 自身免疫性溶血性贫血
degranulation 脱颗粒 drug allergic cytopenia 药物过敏性血细胞减少症
histamine 组胺 Goodpasture syndrome 肺出血肾炎综合征
kininogenase 激肽原酶 myasthenia gravis, MG 重症肌无力
platelet activating factor，PAF 血小板活化因子 soluble immune complex 可溶性免疫复合物
leukotriene，LT 白三烯 deposition 沉积
prostaglandin D2，PGD2 前列腺素 D2 basement membrane 基底膜
smooth muscle contraction 平滑肌收缩 platelet 血小板
capillaries dilatation 毛细血管扩张 edema 水肿
permeability 通透性 necrosis 坏死
gland 腺 vasoactive substances 血管活性物质
hypersecretion 分泌过多 vasopermeability 血管通透性
systemic anaphylaxis 全身性过敏反应 aggregation 聚集
localized anaphylaxis 局部过敏反应 infiltration 浸润
anaphylactic shock 过敏性休克 blood clotting system 凝血系统
urticaria 荨麻疹 microthrombosis 微血栓形成
respiratory tract 呼吸道 ischemia 缺血
allergic rhinitis 变应性（过敏性）鼻炎 serum sickness 血清病
 rheumatoid arthritis 类风湿性关节炎 lesion 损害
systemic lupus erythematosus，SLE 系统性红斑狼疮 tuberculosis 肺结核
mononuclearcell 单个核细胞 contact dermatitis 接触性皮炎
exudation 渗出
post-streptococcal glomerulonephritis 链球菌感染后肾小球肾炎
Grave’s disease 甲状腺功能亢进症，毒性弥漫性甲状腺肿

Section 18
autoimmunity 自身免疫 gender factors 性别因素
autoimmune disease 自身免疫性疾病 abnormality 异常
autoantibody 自身抗体 autoimmune cytopenia 自身免疫性血细胞减症
autoreactive T cell 自身反应性 T 细胞 autoimmune anemia 自身免疫性贫血
molecular mimicry 分子模拟 pernicious anemia 恶性贫血
sympathetic ophthalmia 交感性眼炎 myasthenia gravis，MG 重症肌无力
rheumatoid factor, RF 类风湿因子 multiple sclerosis，MS 多发性硬化症
dominant epitope/primary epitope 优势表位/原发表位 systemic lupus erythematosus, SLE 系统性红斑狼疮
cryptic epitope/secondary epitope 隐蔽表位/继发表位 rheumatoid arthritis, RA 类风湿性关节炎
epitope spreading 表位扩展 exacerbate 加重，恶化
organ specific autoimmune disease 器官特异性自身免疫性疾病
systemic autoimmune disease 全身性自身免疫性疾病
insulin-dependent diabetes mellitus，IDDM 胰岛素依赖型糖尿病
autoimmune thrombocytopenic purpura 自身免疫性血小板减少性紫癜
autoimmune neutropenia 自身免疫性中性粒细胞减少症

Section 19
immunodeficiency disease，IDD 免疫缺陷病 malignant tumor 恶性肿瘤
congenital hypoplasia 先天性发育不全 immunosuppressive drug 免疫抑制药物
postnatal 出生后的 radiographic exposure 放射线照射
bactericidal activity 杀菌活性 opportunistic infection 机会性感染
adenosine deaminase，ADA 腺苷脱氨酶 central nervous system 中枢神经系统
malnutrition 营养不良 degeneration 变性，退化
primary immunodeficiency disease，PIDD 原发性免疫缺陷病
congenital immunodeficiency disease，CIDD 先天性免疫缺陷病
acquired immunodeficiency disease，AIDD 获得性免疫缺陷病
X-linked agammaglobulinaemia，XLA X 连锁无丙种球蛋白血症
common variable immunodeficiency, CVID 普通变异型免疫缺陷病
chronic granulomatous disease, CGD X 连锁慢性肉芽肿病
Hereditary angioneurotic edema 遗传性血管神经性水肿
paroxysmal nocturnal hemoglobinuria，PNH 阵发性夜间血红蛋白尿
Wiskott-Aldrich syndrome, WAS 伴湿疹血小板减少的免疫缺陷病
human immunodeficiency virus，HIV 人类免疫缺陷病毒
acquired immunodeficiency syndrome，AIDS 获得性免疫缺陷综合征

Section 20
tumor immunology 肿瘤免疫学 tumor specific antigen，TSA 肿瘤特异性抗原
tumor antigen 肿瘤抗原 tumor-associated antigen，TAA 肿瘤相关抗原
neoantigen 新抗原 tumor rejection antigen，TRA 肿瘤排斥抗原
genesis 发生 antigenic deletion 抗原缺失
canceration 癌变 antigenic modulation 抗原调变
overexpression 过度表达 tumor microenvironments 肿瘤微环境
oncogene 原癌基因 immunodiagnosis 免疫诊断
oncogenic virus 致癌病毒 immunotherapy 免疫治疗
fetal antigen 胚胎抗原 immunoprophylaxis 免疫预防
glycosylation 糖基化
tumor cell 肿瘤细胞
tumor specific transplantation antigen，TSTA 肿瘤特异性移植抗原
myeloid-derived suppressor cells，MDSC 髓源性抑制性细胞

Section 21
transplantation immunology 移植免疫 host versus graft reaction，HVGR 宿主抗移植物反应
graft 移植物 graft versus host reaction(GVHR) 移植物抗宿主反应
autologous transplantation 自体移植 hyperacute rejection 超急性排斥反应
syngeneic transplantation 同系移植 acute rejection 急性排斥反应
allogeneic transplantation 同种（异体）移植 chronic rejection 慢性排斥反应
xenogeneic transplantation 异种移植 pregnancy 妊娠
rejection 排斥 hemodialysis 血液透析
alloantigen 同种抗原 chronic vascular rejection，VCR 血管慢性排斥
recipient 受者 degeneration 退行性变
donor 供者
major histocompatibility antigens，MHC 主要组织相容性抗原
minor histocompatibility antigens，mH 次要组织相容性抗原
Section 23
immunoprophylaxis 免疫预防 conjugate vaccine 结合疫苗
immunotherapy 免疫治疗 DNA vaccine DNA 疫苗
artificial active immunization 人工主动免疫 recombinant vector vaccine 重组载体疫苗
artificial passive immunization 人工被动免疫 synthetic peptide vaccine 合成肽疫苗
vaccine 疫苗 edible vaccine 食用疫苗
antitoxin 抗毒素 mucosal vaccine 粘膜疫苗
inoculate/inoculation 接种 transdermal vaccine 透皮疫苗
inactivated vaccine 灭活疫苗 therapeutic vaccine 治疗性疫苗
live-attenuated vaccine 减毒活疫苗 planed Immunization 计划免疫
toxoid 类毒素
subunit vaccine 亚单位疫苗