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1. Introduction to Immunology
Definition and Scope of Immunology:
Immunology is the study of the immune system, a complex network of cells, tissues, and
molecules that defend the body against pathogens (e.g., bacteria, viruses) while maintaining
tolerance to self-tissues. Its scope spans:

 Health Applications: Vaccine development, allergy management, cancer

immunotherapy.

 Disease Mechanisms: Autoimmune disorders (e.g., lupus, type 1 diabetes),

immunodeficiencies (e.g., HIV/AIDS).

 Research Frontiers: Understanding microbiome interactions, engineered immune

therapies (e.g., CAR-T cells).

Innate vs. Adaptive Immunity

Feature Innate Immunity Adaptive Immunity

Response Time Immediate (minutes/hours) Delayed (days)

Specificity Non-specific (recognizes broad Highly specific (targets unique

pathogen patterns) antigens)

Memory No memory Long-term memory (secondary

responses)

Key Barriers (skin), phagocytes, NK cells, B cells, T cells, antibodies

Components cytokines

Synergy:

 Innate immunity activates adaptive responses (e.g., dendritic cells present antigens
to T cells).

 Adaptive immunity enhances innate mechanisms (e.g., antibodies tag pathogens for
phagocytosis).

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 Cells, Organs, and Tissues of the Immune System

A. Major Immune Cells:

1. Innate Immune Cells:

o Phagocytes: Neutrophils (bacterial killers), macrophages ("big eaters"),

dendritic cells (antigen presenters).

o Natural Killer (NK) Cells: Destroy virus-infected and cancerous cells.

o Mast Cells/Basophils: Mediate allergic responses.

2. Adaptive Immune Cells:

o B Cells: Produce antibodies.

o T Cells:

 Helper T cells (CD4+): Coordinate immune responses.

 Cytotoxic T cells (CD8+): Kill infected cells.

 Regulatory T cells (Tregs): Suppress excessive immunity.

B. Lymphoid Organs:

1. Primary (Generative):

o Bone Marrow: Produces B cells and innate immune cells.

o Thymus: Matures T cells (central tolerance eliminates self-reactive T cells).

2. Secondary (Peripheral):

o Spleen: Filters blood, removes old RBCs, and detects bloodborne pathogens.

o Lymph Nodes: Filter lymph, sites of B/T cell activation.

o MALT (Mucosa-Associated Lymphoid Tissue): Guards mucosal surfaces (e.g.,

gut, lungs).

Overview of Immunological Memory and Immune Tolerance

A. Immunological Memory:

 Mechanism: Memory B and T cells persist after an infection, enabling faster, stronger
responses upon re-exposure.

 Importance: Basis for vaccines (e.g., measles vaccine primes memory cells without
causing disease).

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  Example: Secondary antibody response produces IgG (more effective) instead of IgM.

B. Immune Tolerance:

 Definition: Prevents immune attacks on self-tissues.

 Mechanisms:

1. Central Tolerance:

 Occurs in thymus (T cells) and bone marrow (B cells).

 Self-reactive lymphocytes are deleted via apoptosis.

2. Peripheral Tolerance:

 Anergy: Functional inactivation of self-reactive lymphocytes.

 Tregs: Suppress autoimmune responses.

 Antigen Sequestering: Barriers (e.g., blood-brain) hide self-antigens.

Failure of Tolerance:

 Autoimmune diseases (e.g., rheumatoid arthritis) occur when self-tolerance breaks

down.

Key Takeaways:

 Innate immunity provides rapid, broad defense; adaptive immunity offers targeted,
memory-driven protection.

 Lymphoid organs are critical for immune cell development and activation.

 Immunological memory enables lifelong protection; tolerance prevents self-

destruction.

Study Tips:

 Use mnemonics: "T cells mature in the Thymus, B cells in Bone marrow."

 Relate concepts to real-world examples (e.g., flu vaccine → memory cells; lupus →
tolerance failure).

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 2. Cells and Organs of the Immune System

Detailed Breakdown

Primary Lymphoid Organs

1. Bone Marrow

 Function:

o Hematopoiesis: Production of all blood cells (red blood cells, platelets, and
immune cells) from hematopoietic stem cells (HSCs).

o B Cell Development: B lymphocytes mature here through stages (pro-B →

pre-B → immature B cells).

 Key Features:

o Stroma: Supportive tissue with cytokines (e.g., IL-7) critical for differentiation.

o Compartments: Red marrow (active in hematopoiesis) vs. yellow marrow

(fatty, inactive).

2. Thymus

 Function:

o T Cell Maturation: Naive T cells (thymocytes) undergo selection to eliminate

self-reactive cells.

 Key Processes:

o Positive Selection: Only T cells that recognize self-MHC molecules survive.

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 o Negative Selection: Apoptosis of T cells that bind strongly to self-antigens
(prevents autoimmunity).

 Structure:

o Cortex: Immature thymocytes interact with cortical epithelial cells.

o Medulla: Mature T cells interact with medullary epithelial cells expressing

tissue-specific antigens.

 Involution: Shrinks with age, reducing T cell production.

Secondary Lymphoid Organs

1. Spleen

 Function:

o Blood Filtration: Removes old/damaged RBCs and pathogens.

o Immune Activation: Initiates adaptive responses to bloodborne antigens.

 Structure:

o Red Pulp: Macrophages phagocytose RBCs and pathogens.

o White Pulp:

 Periarteriolar Lymphoid Sheath (PALS): T cell zone.

 Follicles: B cell zones (germinal centers during activation).

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 2. Lymph Nodes

 Function:

o Lymph Filtration: Traps antigens from tissues via afferent lymphatic vessels.

o Immune Activation: Site of B/T cell interaction and clonal expansion.

 Structure:

o Cortex: B cell follicles (primary and secondary).

o Paracortex: T cell zone with dendritic cells.

o Medulla: Plasma cells and memory cells.

 High Endothelial Venules (HEVs): Entry point for circulating lymphocytes.

3. MALT (Mucosa-Associated Lymphoid Tissue)

 Function: Immune surveillance at mucosal surfaces (gut, respiratory tract, urogenital

tract).

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  Types:

o GALT (Gut-Associated): Peyer’s patches, appendix.

o BALT (Bronchus-Associated).

o NALT (Nasal-Associated): Tonsils, adenoids.

 Key Features:

o M Cells: Specialized epithelial cells that sample antigens for immune cells.

Cells of the Immune System

A. Hematopoiesis and Stem Cells

 (HSCs):

o Pluripotent: Differentiate into myeloid (innate cells) or lymphoid (adaptive

cells) lineages.

o Regulation: Controlled by cytokines (e.g., GM-CSF, G-CSF, IL-3).

 Lineages:

o Myeloid: Gives rise to neutrophils, monocytes, macrophages, dendritic cells,

mast cells, eosinophils, basophils.

o Lymphoid: Produces T cells, B cells, NK cells.

B. Innate Immune Cells

1. Macrophages:

o Function: Phagocytosis, cytokine secretion (e.g., TNF-α), antigen

presentation.

o Types:

 Resident (e.g., Kupffer cells in liver, microglia in brain).

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  Inflammatory (recruited to sites of infection).

2. Neutrophils:

o Function: First responders to infection; phagocytose bacteria, release NETs

(Neutrophil Extracellular Traps).

o Short-lived: Die after phagocytosis, forming pus.

3. Dendritic Cells (DCs):

o Function: Bridge innate and adaptive immunity; present antigens to T cells via
MHC molecules.

o Types:

 Conventional DCs: Migrate to lymph nodes after antigen capture.

 Plasmacytoid DCs: Produce type I interferons during viral infections.

4. Natural Killer (NK) Cells:

o Function: Kill virus-infected or cancerous cells via perforin/granzyme release.

o Activation: Balance of activating (e.g., NKG2D) and inhibitory receptors (e.g.,

KIRs).

C. Adaptive Immune Cells

1. T Cells:

o CD4+ Helper T Cells:

 Subtypes: Th1 (activate macrophages), Th2 (help B cells), Th17

(mucosal immunity), Tfh (follicular helper cells).

 Cytokines: IL-2, IFN-γ, IL-4, IL-17.

o CD8+ Cytotoxic T Cells:

 Function: Kill infected/cancerous cells via perforin and Fas/FasL

pathways.

o Regulatory T Cells (Tregs):

 Marker: FOXP3+.

 Function: Suppress immune responses to prevent autoimmunity.

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 2. B Cells:

o Function: Produce antibodies; act as antigen-presenting cells (APCs).

o Activation: Requires Tfh cells (germinal center reaction) or T-independent

antigens (e.g., polysaccharides).

o Memory B Cells: Long-lived cells for rapid secondary responses.

3. Plasma Cells:

o Function: Differentiated B cells that secrete large amounts of antibodies (e.g.,

IgG, IgA).

o Survival: Short-lived (inflammation) vs. long-lived (bone marrow niches).

Key Concepts & Clinical Correlations

 Hematopoietic Disorders:

o Aplastic Anemia: Bone marrow failure → pancytopenia.

o Leukemia: Cancer of HSCs or lymphoid/myeloid progenitors.

 Thymic Disorders:

o DiGeorge Syndrome: Thymic hypoplasia → T cell deficiency.

 Splenic Dysfunction:

o Asplenia: Increased risk of encapsulated bacterial infections

(e.g., Streptococcus pneumoniae).

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 Summary Table: Immune Cells

Cell Type Origin Key Function Key Markers

Macrophage Bone Marrow Phagocytosis, cytokine release CD14, CD68

Neutrophil Bone Marrow Early phagocytosis, NET formation CD66b, MPO

Dendritic Cell Bone Marrow Antigen presentation to T cells CD11c, MHC-II

NK Cell Bone Marrow Killing infected/cancer cells CD56, CD16 (FcγRIII)

CD4+ T Cell Thymus Coordinate immune responses CD3, CD4

CD8+ T Cell Thymus Cytotoxicity CD3, CD8

B Cell Bone Marrow Antibody production, APC function CD19, CD20, BCR

Plasma Cell Bone Marrow Antibody secretion CD138, Blimp-1

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 Innate Immunity (First Line of Defense):

Innate immunity serves as the body's immediate and non-specific defense against
pathogens. It comprises physical barriers, chemical defenses, cellular components, and
molecular mechanisms that work synergistically to prevent infection and eliminate invaders.
Below is a detailed breakdown:

1. Physical Barriers

A. Skin

 Structure:

o Epidermis: Outer layer of keratinized, dead cells that shed continuously,

removing pathogens.

o Dermis: Contains sweat glands and sebaceous glands that secrete

antimicrobial substances.

 Defense Mechanisms:

o Acidic pH: Sweat (pH 4–6) and sebum (fatty acids) inhibit bacterial growth.

o Microbiota: Commensal bacteria (e.g., Staphylococcus epidermidis) compete

with pathogens for resources.

B. Mucosal Surfaces

 Respiratory Tract:

o Mucus: Traps pathogens; ciliated epithelial cells propel mucus upward for
expulsion (e.g., coughing).

o Nasal Hairs: Filter large particles.

 Gastrointestinal Tract:

o Stomach Acid: HCl (pH ~2) denatures proteins and kills most microbes.

o Peristalsis: Rapid movement of intestinal contents limits microbial

colonization.

o Gut Microbiome: Beneficial bacteria (e.g., Lactobacillus) outcompete

pathogens and produce antimicrobial peptides.

 Urinary Tract:

o Flushing Mechanism: Frequent urination expels microbes.

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 o Low pH: Urine acidity inhibits bacterial growth.

2. Chemical Barriers

A. Enzymes

 Lysozyme: Found in tears, saliva, and mucus; breaks down peptidoglycan in bacterial
cell walls.

 Pepsin: In gastric juice; digests microbial proteins.

 Secretory Phospholipase A2: In saliva and tears; hydrolyzes bacterial membranes.

B. Antimicrobial Peptides

 Defensins:

o α-Defensins: Produced by neutrophils and Paneth cells (intestines); form

pores in microbial membranes.

o β-Defensins: Secreted by epithelial cells (e.g., skin, respiratory tract).

 Cathelicidins (e.g., LL-37): Disrupt microbial membranes and neutralize endotoxins.

 Histatins: In saliva; antifungal properties.

3. Pattern Recognition Receptors (PRRs)

PRRs detect Pathogen-Associated Molecular Patterns (PAMPs) and Damage-Associated

Molecular Patterns (DAMPs).

PRR Family Examples Ligands Location

Toll-like Receptors (TLRs) TLR4 (cell LPS (Gram-negative bacteria) Cell surface
surface)

TLR3 Double-stranded RNA (viruses) Endosomes

(endosome)

NOD-like Receptors NLRP3 (cytosol) Bacterial peptidoglycan, ATP Cytoplasm

(NLRs)

RIG-I-like Receptors RIG-I (cytosol) Viral RNA (e.g., influenza, Cytoplasm

(RLRs) hepatitis)

C-type Lectin Receptors Dectin-1 β-glucans (fungi) Cell surface

(CLRs)

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 Outcome: PRR activation triggers signaling pathways (e.g., NF-κB, IRF3) leading to cytokine
production and inflammation.

4. Complement System

Three pathways converge to enhance pathogen clearance:

Pathway Activation Trigger Key Outcomes

Components

Classical Antigen-antibody C1q, C2, C4 Opsonization (C3b), inflammation

complexes (C3a/C5a), MAC formation (C5b-9)

Lectin Mannose-binding MBL, MASP Same as classical

lectin (MBL) enzymes

Alternative Spontaneous C3 Factor B, Factor Amplifies complement activation

hydrolysis D

Functions:

 Opsonization: C3b coats pathogens for phagocytosis.

 Inflammation: C3a/C5a recruit immune cells (chemotaxis).

 Lysis: MAC forms pores in pathogen membranes.

5. Inflammation and Phagocytosis

A. Inflammatory Response

1. Vasodilation: Histamine and prostaglandins increase blood flow.

2. Increased Permeability: Plasma proteins (e.g., complement) enter tissues.

3. Leukocyte Recruitment:

o Neutrophils: First responders (6–12 hours).

o Macrophages: Arrive later (24–48 hours).

4. Resolution: Anti-inflammatory cytokines (e.g., IL-10) dampen the response.

B. Phagocytosis

1. Chemotaxis: Phagocytes migrate toward chemokines (e.g., IL-8).

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 2. Adherence: Enhanced by opsonins (C3b, IgG).

3. Ingestion: Pathogen engulfed into a phagosome.

4. Digestion:

o Phagolysosome Formation: Fusion with lysosomes containing lysozyme, ROS,

and proteases.

o Reactive Oxygen Species (ROS): NADPH oxidase generates superoxide

radicals.

Phagocytes:

 Neutrophils: Short-lived; primary responders.

 Macrophages: Long-lived; present antigens to adaptive immunity.

 Dendritic Cells: Link innate and adaptive immunity.

6. Cytokines and Chemokines

A. Pro-Inflammatory Cytokines

 IL-1β:

o Source: Macrophages, epithelial cells.

o Role: Induces fever, activates endothelium for leukocyte adhesion.

 TNF-α:

o Source: Macrophages, T cells.

o Role: Promotes inflammation, induces apoptosis in infected cells.

B. Interferons (IFNs)

 Type I (IFN-α/β):

o Source: Virus-infected cells.

o Role: Induce antiviral proteins (e.g., PKR, RNase L); upregulate MHC-I.

 Type II (IFN-γ):

o Source: NK cells, Th1 cells.

o Role: Activates macrophages; enhances antigen presentation.

C. Chemokines

 IL-8 (CXCL8): Attracts neutrophils.

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  MCP-1 (CCL2): Recruits monocytes/macrophages.

 RANTES (CCL5): Chemotactic for T cells and eosinophils.

Clinical Correlations

 Complement Deficiencies: Increased susceptibility to Neisseria infections (e.g., C5–

C9 deficiency).

 TLR4 Mutations: Linked to endotoxin hyporesponsiveness (Gram-negative sepsis

risk).

 Chronic Granulomatous Disease: NADPH oxidase defect → recurrent bacterial/fungal

infections.

 Cystic Fibrosis: Thick mucus impairs ciliary function, leading to chronic lung
infections.

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 Adaptive Immunity (Antigen-Specific Defense):

Adaptive immunity is a highly specific defense mechanism that targets pathogens through
specialized cells (T and B lymphocytes) and immunological memory. Below is a structured
breakdown of its components:

1. Antigen Recognition and Processing

 Antigens: Foreign molecules (e.g., viral proteins, bacterial toxins) recognized by

immune cells.

 Antigen Processing:

o Endogenous Pathway:

 MHC-I Presentation: Intracellular antigens (e.g., viral proteins) are

degraded by proteasomes, loaded onto MHC-I molecules, and
displayed on all nucleated cells.

 Recognition by CD8+ T Cells: Cytotoxic T cells (CTLs) detect antigen-

MHC-I complexes to eliminate infected cells.

o Exogenous Pathway:

 MHC-II Presentation: Extracellular antigens (e.g., bacteria) are

engulfed by antigen-presenting cells (APCs), degraded in lysosomes,
and loaded onto MHC-II molecules.

 Recognition by CD4+ T Cells: Helper T cells (Th) detect antigen-MHC-II

complexes to coordinate immune responses.

2. Major Histocompatibility Complex (MHC)

Feature MHC-I MHC-II

Structure α-chain + β2- α-chain + β-chain

microglobulin

Antigen Source Intracellular Extracellular (exogenous)

(endogenous)

Presenting All nucleated cells Professional APCs (DCs, macrophages, B cells)

Cells

T Cell Partner CD8+ T cells (CTLs) CD4+ T cells (Th cells)

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 3. T Cell-Mediated Immunity (Cell-Mediated Immunity, CMI)

A. T Cell Activation

 Antigen Presentation: APCs display antigen-MHC complexes to T cells.

 Co-stimulation:

o B7 (CD80/86) on APCs binds CD28 on T cells (required for full activation).

o Without co-stimulation, T cells become anergic (unresponsive).

 Cytokine Signals: Determine T cell differentiation (e.g., IL-12 → Th1; IL-4 → Th2).

B. T Helper (Th) Cell Subsets

Subset Key Function Target Pathogens

Cytokines

Th1 IFN-γ, IL-2 Activate macrophages, promote Intracellular (e.g., Mycobacterium

CTL responses tuberculosis)

Th2 IL-4, IL-5, IL- Stimulate B cells for antibody Extracellular (e.g., helminths)
13 production

Th17 IL-17, IL-22 Recruit neutrophils, defend Fungi, extracellular bacteria

mucosal barriers

Treg IL-10, TGF-β Suppress immune responses, Self-tolerance maintenance

prevent autoimmunity

C. Cytotoxic T Lymphocytes (CTLs)

 Function: Kill infected/cancerous cells via perforin (pore formation)

and granzymes (induce apoptosis).

 Mechanism: Recognize antigen-MHC-I complexes; release cytotoxic granules upon

contact.

4. B Cell-Mediated Immunity (Humoral Immunity)

A. B Cell Activation

 Antigen Recognition: B cell receptors (BCRs) bind antigens directly.

 T Cell Help:

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 o B cells present antigen-MHC-II to Th2 cells.

o Th2 cells secrete IL-4/IL-21, driving B cell proliferation and class-switching.

 Clonal Selection: Activated B cells differentiate into plasma cells (antibody factories)
and memory B cells.

1. Structure of Antibodies

Antibodies (immunoglobulins) are Y-shaped glycoproteins produced by B cells. Their

structure enables antigen binding and immune effector functions:

 Heavy and Light Chains:

o Heavy Chains: Two identical long polypeptide chains (determine antibody

class: IgG, IgA, etc.).

o Light Chains: Two identical short polypeptide chains (κ or λ types).

o Linked by disulfide bonds and non-covalent interactions.

 Fab (Fragment antigen-binding) Region:

o Located at the "arms" of the Y.

o Contains variable regions (antigen-binding sites) for specificity.

 Fc (Fragment crystallizable) Region:

o Stem of the Y.

o Mediates effector functions (e.g., binding to immune cells, complement

activation).

Key Features:

 Valence: Number of antigen-binding sites (e.g., IgG = 2; IgM pentamer = 10).

 Hinge Region: Provides flexibility for antigen binding.

2. Types of Immunoglobulins

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 Class Structure Distribution Key Functions

IgG Monomer Blood, tissues, placenta - Neutralizes pathogens/toxins.

- Opsonizes for phagocytosis.
- Activates complement.

IgA Monomer (serum) or Mucosal surfaces (gut, - Prevents pathogen attachment

dimer (secretions) saliva, breast milk) to mucosal surfaces.
- Passive immunity via
breastfeeding.

IgM Pentamer Blood, B cell surface - First antibody in primary

response.
- Agglutinates pathogens.
- Activates complement.

IgE Monomer Bound to mast - Triggers allergic reactions

cells/basophils (histamine release).
- Defense against helminths.

IgD Monomer B cell surface - B cell receptor (BCR) for

antigen recognition.

3. Antigen-Antibody Reactions

Antibodies neutralize or eliminate pathogens through diverse mechanisms:

A. Agglutination

 Mechanism: Antibodies (e.g., IgM) cross-link pathogens or particles into clumps.

 Outcome: Facilitates phagocytosis (e.g., clumped bacteria are easier to engulf).

B. Precipitation

 Mechanism: Antibodies bind soluble antigens (e.g., toxins) to form insoluble

complexes.

 Outcome: Complexes are cleared by phagocytes.

C. Neutralization

 Mechanism: Antibodies block pathogen/toxin binding to host cells (e.g., IgG

neutralizes viruses).

 Outcome: Prevents infection or toxin activity.

D. Opsonization

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  Mechanism: Antibodies (e.g., IgG) coat pathogens via Fab regions; Fc regions bind
phagocyte receptors.

 Outcome: Enhances phagocytosis ("tagging" for destruction).

4. Clinical and Functional Significance

 IgG: Dominant in secondary responses; crosses placenta for neonatal immunity.

 IgM: Key marker of acute infection (e.g., elevated in early COVID-19).

 IgA: Critical for mucosal immunity; deficiency linked to recurrent infections.

 IgE: Elevated in allergies (e.g., asthma, anaphylaxis) and parasitic infections.

 Complement Activation: IgG/IgM trigger the classical pathway, leading to pathogen

lysis.

Key Takeaways

 Antibodies are highly specific due to variable regions but share conserved Fc regions
for effector functions.

 Each immunoglobulin class has unique roles in immunity, from pathogen

neutralization (IgG) to allergic responses (IgE).

 Antigen-antibody interactions (agglutination, neutralization) are foundational to

diagnostics (e.g., ELISA) and vaccines.

Immunological Disorders and Diseases:

1. Hypersensitivity Reactions

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 Hypersensitivity reactions occur when the immune system overreacts to antigens, causing
tissue damage. They are classified into four types:

Type Mechanism Examples Key Features

I IgE-mediated (mast Allergies (pollen, food), Rapid onset (minutes); histamine

cell degranulation) Anaphylaxis release causes urticaria,
bronchoconstriction.

II IgG/IgM-mediated Graves' disease, Antibodies target cell-surface

cytotoxicity Hemolytic disease of antigens (e.g., TSH receptor in
the newborn Graves' disease).

III Immune complex Systemic Lupus Antigen-antibody complexes deposit

deposition Erythematosus (SLE), in tissues, triggering inflammation
Serum sickness (e.g., glomerulonephritis).

IV T cell-mediated Contact dermatitis Delayed onset (24–72 hrs); involves

(delayed) (poison ivy), Tuberculin CD4+/CD8+ T cells and macrophages.
skin test

2. Autoimmune Diseases

Autoimmunity arises when the immune system attacks self-antigens. Key examples include:

Disease Target Antigen/Mechanism Clinical Features

Systemic Lupus Anti-dsDNA, anti-Sm antibodies Butterfly rash, arthritis, renal

Erythematosus (SLE) dysfunction, fatigue.

Rheumatoid Arthritis Autoantibodies (e.g., RF, anti- Symmetrical joint

(RA) CCP) attack joints inflammation, morning
stiffness.

Multiple Sclerosis (MS) T cells attack myelin sheath in Numbness, muscle weakness,
CNS vision problems.

Type 1 Diabetes Destruction of pancreatic β-cells Hyperglycemia, dependence

by T cells on insulin therapy.

3. Immunodeficiency Disorders

Immunodeficiencies result from impaired immune function, leading to recurrent infections.

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 A. Primary (Congenital) Immunodeficiencies

 Severe Combined Immunodeficiency (SCID):

o Defect: Absence of functional T/B cells.

o Example: "Bubble boy" disease; treated with bone marrow transplantation.

 Bruton’s Agammaglobulinemia:

o Defect: Mutation in BTK gene → no mature B cells.

o Features: Recurrent bacterial infections (low IgG).

B. Secondary (Acquired) Immunodeficiencies

 HIV/AIDS:

o Mechanism: CD4+ T cell depletion by HIV.

o Outcome: Opportunistic infections (e.g., Pneumocystis pneumonia).

 Cancer-Induced Immunodeficiency:

o Causes: Leukemia, lymphoma, or chemotherapy.

o Features: Neutropenia, increased infection risk.

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