TABLE OF CONTENTS

Immunology 1.
2.
Lymphoid Tissue
Innate vs Adaptive Immunity
3. Inflammatory Response
4. Cytokines
5. T-cells
6. B-cells
7. Antibodies
8. Complement
9. Vaccinations
10. Immunodeficiency Syndromes
11. Hypersensitivities
12. Blood Transfusion Reactions
13. Transplant Rejection
 OUTLINE
1. Overview
● A. Types of Lymphoid Tissue

Immunology: 2. Primary Lymphoid Organs

●
●
A. Bone Marrow
B. Thymus

Lymphoid Tissue 3. Secondary Lymphoid Organs

●
●
A. Spleen
B. Lymph Node
● C. Peyer’s Patches
● D. Tonsils
 Immunology: Lymphoid Tissue Bootcamp.com

• Primary
• Types: Bone marrow, Thymus
• Lymphocyte formation and development
• Secondary
• Types: Spleen, Lymph node, Peyer’s patches, Tonsils
• Lymphocyte activation and proliferation
 Immunology: Lymphoid Tissue Bootcamp.com

• Bone Marrow:
• Hematopoietic stem cells à Lymphoid lineage à B-cells, T-cells, NK cells
• B-cell proliferation and maturation

GM-
CSF

IL-7 HSC IL-3

Lymphoid Myeloid

Macrophages,
B-cells T-cells NK cells Erythrocytes Platelets Dendritic cells Monocytes Eosinophils Basophils Mast cells

Mature in bone Mature in

marrow thymus
 Immunology: Lymphoid Tissue Bootcamp.com

• Thymus:
• Derived from 3rd pharyngeal pouch
• Encapsulated
• T-cell maturation
• Cortex: Darker staining (↑ lymphocytes)
• Medulla: Lighter staining
• Hassal corpuscles (medulla)
• DiGeorge Syndrome, SCIDà Thymic aplasia
• Myasthenia Gravis à Thymoma
 Immunology: Lymphoid Tissue Bootcamp.com

• Spleen:
• White pulp à Follicles à B-cells
• White pulp à Periarteriolar lymphatic sheaths à T-cells
• Marginal zone à Phagocytic cells, antigen presentation from blood

• Red pulp à Arterioles, Sinusoids, Phagocytic cells

• Age-dependent RBC removal by macrophages
• Asplenia à ↑ Risk of infection w/ encapsulated bacteria à Vaccinate
• Trauma à Rupture
• Hereditary spherocytosis à Splenectomy
• Sickle Cell Disease à Functional asplenia
• IgM production
• Platelet storage

Big 3 Encapsulated Bacteria

Streptococcus Pneumoniae
Haemophiles influenza type b
Neisseria meningitidis
 Immunology: Lymphoid Tissue Bootcamp.com

• Lymph Nodes:
• Cortex à Follicles à B-cells
• Primary follicles = Dense and dormant
• Secondary follicles = Activation, isotype switching, ↑ Infection, ↓ X-linked agammaglobulinemia, ↓ SCID

• Paracortex à T-cells
• High endothelial venules à Lymphocytes enter
• ↑ Viral and fungal infection, ↓ DiGeorge Syndrome

• Medulla à Plasma cells, lymphocytes, macrophages

• Sinuses à Drain lymph out, macrophages
 Immunology: Lymphoid Tissue Bootcamp.com

• Peyer’s Patches
• Ileum
• M-cells à Antigen transport to macrophages
• B-cells à Identify antigens à Plasma cells à IgA
• Tonsils
≣ Item 1 of 13 Test Your Knowledge
Difficulty Rating: ✪✪ Bootcamp.com
Question ID: 0058

A 22-day old male with an uncomplicated prenatal history presents to the emergency department with recent seizure activity and failure to
thrive. Vital signs reveal a temperature of 38.3 ℃ (101℉), respiratory rate of 72 breaths/min, and a heart rate of 164 beats/min. Physical
examination reveals a harsh systolic ejection murmur at the left upper sternal border with a single S2. Initial labs are significant for severe
hypocalcemia. Calcium supplementation and broad-spectrum antibiotics are initiated. Chest X-ray reveals cardiomegaly and an absence of a
thymic shadow.

Tracheal aspirate cultures later grow Enterobacter cloacae. Over the following days, the infant develops pancytopenia and multiorgan failure
with disseminated intravascular coagulation. Despite numerous attempts at medical intervention, the infant would later expire. Biopsies are
obtained and reviewed. Mediastinal soft tissue biopsies fail to reveal significant parathyroid and thymic tissues. Lymph node specimens are
most likely to reveal which of the following findings?

⚪ A. Centrilobular necrosis and massive sinusoidal congestion

⚪ B. Underdevelopment of primary and secondary follicles

⚪ C. Paracortical atrophy

⚪ D. Reactive paracortical hyperplasia

⚪ E. Adipose tissue infiltration and hypocellularity

 OUTLINE
1. Innate Immunity
● A. General Characteristics

Immunology: ●
●
●
B. Innate Response
C. Primary Function
D. Genetic Considerations

Innate vs Adaptive 2. Adaptive Immunity

●
●
A. General Characteristics
B. Adaptive Response

Immunity ●
●
C. Primary Function
D. Genetic Considerations
3. Antigen Presentation
● A. Antigen Presenting Cells
● B. Dendritic Cell à Antigen Presentation
● C. B-cell à Antigen Presentation
 Immunology: Innate vs Adaptive Immunity Bootcamp.com

• General Characteristics:
• Nonspecific
• Speed: Rapid
• Future Response: Equal to initial
• Memory: None
• Antigen ID: Toll-like receptors (TLRs) ß à PAMPs à ↑ NF-kB
• IgM, Complement, lysozyme, lactoferrin, respiratory burst (superoxide radicals, hydrogen peroxide)
• Innate Response:
• Bone marrow à ↑ Neutrophils and other PMNs
• Neutrophils à General response, phagocytosis, oxidative burst
• Eosinophil à Parasitic infection, phagocytosis
• Basophil à Parasitic infection, allergic reaction
• Mast cells à Allergic reaction
• Monocytes à Macrophages à Phagocytosis, antigen presentation
• Monocytes à Dendritic cells à Phagocytosis, antigen presentation
• Natural killer cells
• Primary Function:
• Rapid recognition and resolution of new infectious agent
• Effective vs fungi and parasites
• Genetic Considerations:
• Germline encoded
 Immunology: Innate vs Adaptive Immunity Bootcamp.com

• General Characteristics:
• Specific
• Speed: Slow
• Future Response: Heightened
• Memory: Present after exposure
• Antigen ID: Previous epitope exposure
• IgM à IgA, IgG, IgE
• Adaptive Response:
• T-cells à CD8+, CD4+
• B-cellsà Plasma cells, immunoglobulins
• Primary Function:
• Rapid recognition and resolution of previously encounter infectious agent
• Effective vs robust or frequently encountered pathogens
• Genetic Considerations:
• VDJ recombination, hypervariation
 Immunology: Innate vs Adaptive Immunity Bootcamp.com

• Antigen Presenting Cells (APCs)

• Dendritic cells
• Macrophages
• Monocytes
• B-cells
• Dendritic Cell à Antigen Presentation:
• Dendritic cell phagocytosis of pathogen
• Protein components loaded onto major histocompatibility complex (MHC) receptor I or II
• Antigen presentation to naïve T-cell with matching T-cell receptor (TCR)
• T-cell is activated à Cell-mediated Immunity
• CD4+ TCR binds to MHC II à Cytokine release
• CD8+ TCR binds to MHC I à Destroys APC
• B-cell à Antigen Presentation:
• B-cell phagocytosis of pathogen
• Protein components loaded onto major histocompatibility complex (MHC) receptor II
• Antigen presentation to naïve T-cell in with matching T-cell receptor (TCR)
• B-cell à Class switching à Plasma cell à Humoral Immunity
≣ Item 2 of 13 Test Your Knowledge
Difficulty Rating: ✪✪✪ Bootcamp.com
Question ID: 0059

A researcher is studying the relationship between pattern recognition receptors (PRR) present within host cells and Crohn’s disease. The
PRR, nucleotide-binding oligomerization domain protein 2 (NOD2) has been shown to detect conserved motifs in bacterial peptidoglycans
such as the intracellular muramyl dipeptide and promote activation of host proinflammatory pathways. NOD2 has been known to be highly
expressed in Paneth cells of the small intestine. The researcher attempts to induce mutations to further elucidate the effects of ileal
inflammation on NOD2-deficient mice.

Based on the information above, which of the following would most likely be impaired in NOD2-deficient mice?

⚪ A. NF-κB activity

⚪ B. B7 protein binding to CD28

⚪ C. CD40 membrane receptor activity

⚪ D. Alterations within the heavy chain constant domain of immunoglobulins

⚪ E. Terminal deoxynucleotidyl transferase activity

 OUTLINE
1. Acute Inflammatory Response
● A. Toll-Like Receptors

Immunology: ●
●
●
B. Arachidonic Acid
C. Bradykinin, Hageman Factor XII
D. Inflammatory Cytokines

Inflammation ● E. Damaged Endothelial Cells

2. Neutrophil Migration
● A. Margination
● B. Rolling
● C. Tight Adhesion
● D. Transmigration
3. Disorders of Leukocyte Migration
● A. Leukocyte Adhesion Deficiency
● B. Chediak-Higashi Syndrome
4. Chronic Inflammatory Response
● A. Chronic Inflammation
● B. Granulomas
 Immunology: Inflammation Bootcamp.com

• Toll-Like Receptors (TLRs):

• PRRs recognize PAMPs and DAMPs à Triggers inflammatory response
• Ex. TLR4 à LPS
• Co-receptor for TLR4: CD14
• Expressed in phagocytes of innate immune system
• NF-kB nuclear translocation
• Arachidonic Acid:
• Lipooxygenase pathway à Leukotrienes à LTB4 à ↑ Neutrophil chemotaxis
• Cyclooxygenase pathway à ↑ Prostaglandins à ↑ TXA2
• Complement:
• C3a, C4a à ↑ Histamine release from mast cells à ↑ Vasodilation
• C3b à Opsonization
• C5a à ↑ Neutrophil chemotaxis and ↑ Histamine release from mast cells à ↑ Vasodilation
• C5b-9 Membrane Attack Complex à Pathogen cell lysis
• Bradykinin, Hageman Factor XII:
• ↑ Vasodilation
• ↑ Vascular permeability
• ↑ Pain sensitivity
• Inflammatory Cytokines:
• IL-1, TNF-⍺, IL-6 à Acute Inflammatory process
• IL-8 à ↑ Neutrophil chemotaxis, ongoing inflammation
• IL-1, TNF à ↑ T setpoint, ↑ E-selectin, ICAM-1 on endothelium
• Damaged Endothelial Cells:
• ↑ Nitric oxide à ↑ Vasodilation
• ↑ Adhesion proteins à ↑ Neutrophil extravasation
 Immunology: Inflammation Bootcamp.com

• Margination:
• ↑ Vascular permeability à Hemoconcentration à ↑ Neutrophil contact with endothelium
• Rolling:
• Neutrophil: Sialyl LewisX
• Endothelium: E-selectin, P-selectin
• Tight Adhesion:
• Neutrophil: LFA-1 (CD11a/CD18), Mac1 (CD11b/CD18)
• Endothelium: ICAM-1 (CD54)
• Transmigration:
• Neutrophil: PECAM-1 (CD31)
• Endothelium: PECAM-1 (CD31)
• Driven by chemotaxis (LTB4, IL-8, C5a)
 Immunology: Inflammation Bootcamp.com

• Leukocyte Adhesion Deficiency:

• LAD type 1: Absence of LFA-1 (CD18) (or Mac-1 on macrophages)
• Unable to have tight adhesion
• Presentation: Recurrent infections with absence of pus
• Impaired wound healing
• Umbilical cord delayed detachment
• Chediak-Higashi Syndrome:
• Impaired microtubule polymerization à ↓ Neutrophil chemotaxis
• Lysosomal dysfunction à Enlarged vesicles, non-functioning lysosomes
• Autosomal recessive, LYST gene defect
• Presentation: Recurrent infections, partial albinism, peripheral neuropathy
• Giant cytoplasmic granules
 Immunology: Inflammation Bootcamp.com

• Chronic Inflammation:
• Fibrosis, Angiogenesis
• Tuberculosis classic
• IFN-ɣ: Secreted by Th1 cells, activates macrophages to ↑ inflammatory response
• IL-4, IL-13: Secreted by Th2 cells, activate macrophages to ↓ inflammatory response
• FGF, VEGF: ↑ Angiogenesis
• TGF-β: ↑ Angiogenesis, Fibrosis
• PDGF: ↑ Fibroblast collagen synthesis
• Granulomas:
• APC à Th cells (CD4+) + IL-12 à Th1 cells
• Th1 cells à IFN-ɣ, TNF-⍺ à Macrophage activation
• Macrophages à TNF-⍺
• Granuloma maintained by IL-12 and TNF-⍺
• Multinucleated giant cells, fibroblasts, lymphocytes, epithelioid cells
• Caseating: Central necrotic core (TB, fungal infections)
• Non-caseating: Absence of necrotic core (Sarcoidosis, Beryllium)
≣ Item 3 of 13 Test Your Knowledge
Difficulty Rating: ✪✪ Bootcamp.com
Question ID: 0060

A 1-month-old male presents with family to a pediatric ward in rural Chile for irritability. Physical examination reveals tenderness and
erythema at the umbilical stump with serosanguinous drainage. Notably, the umbilical cord remains attached from birth. Induration is also
noted along the surrounding tissues. Otoscopic examination demonstrates a bulging right tympanic membrane with opacification and a loss
of light reflex. Initial laboratory evaluation is shown below.

Hemoglobin: 16.5 g/dL

Leukocyte count: 45,500/mm3
Platelet count: 185,000/mm3
C-reactive protein: Elevated
Nitroblue tetrazolium dye reduction test: Positive

Which of the following are most likely linked to the underlying condition in this infant?

⚪ A. LYST gene defect

⚪ B. Impaired microtubule polymerization

⚪ C. Impaired superoxide production

⚪ D. Absence of CD18 (LFA-1)

⚪ E. HAX1 gene defect

 OUTLINE
1. Proinflammatory Cytokines
● A. Acute Inflammatory Response

Immunology: ●
●
B. Proliferative Response
C. Th1 Response
2. Additional Cytokines

Cytokines ●
●
●
A. Th2 Response
B. Class Switching Cytokines
C. Allergic and Parasitic Response
● D. Treg and Th17 Response
 Immunology: Cytokines Bootcamp.com

• Acute Inflammatory Response:

• PRRs à PAMPs, DAMPs
• ↑ NF-kB
• Initial Response: IL-1, IL-6, TNF à Acute reactants
• ↑ Expression of endothelial adhesion molecules
• Neutrophil Chemotaxis à IL-8, LTB4, C5a
• Proliferative Response:
• IL-2 à ↑ Proliferation of immune cells
• Ag binds to TCR à IL-2 à Autocrine action
• IL-3 à ↑ Hematopoiesis
• Th1 Response:
• Th1 response à Cell-mediated response
• Macrophage à Th1 stimulation via IL-2
• Th1 cells à Macrophage stimulation via IFN-ɣ
• IFN-⍺, IFN-β à Released from virally infected cells
• IFN-ɣ à Activation of macrophages and CD8+ T-cells
 Immunology: Cytokines Bootcamp.com

• Th2 Response:
• Th2 response à Humoral-mediated
• IL4, IL-5, IL-10, IL-13
• Secreted by Th2 cells, Treg cells, and macrophages
• Class Switching Cytokines:
• IL-4 à Th2 à ↑ IgE, IgG
• IL-5 à ↑ IgA, Eosinophils
• IL-13 à ↑ IgE
• Allergic and Parasitic Response:
• IL-4, IL-5, IL-10, IL-13, IL-17
• Eosinophils, Basophils, Mast cells
• Treg, Th17 Response:
• TGF-β, IL-10 à Treg à Prevent autoimmunity à ↓ Immune response
• TGF-β à Th17 à IL-17 à ↑ Neutrophil function
≣ Item 4 of 13 Test Your Knowledge
Difficulty Rating: ✪✪ Bootcamp.com
Question ID: 0061

A 74-year-old female presents to the emergency department with acute onset diplopia and severe unilateral right-sided headache. Her past
medical history is significant for hypertension, hyperlipidemia, and osteopenia. The patient reports that she has had 10 lbs (4.5 kg) of weight
loss over the past 3 months and has also had increased fatigue and symmetric bilateral shoulder, hip, and neck pain that is worse in the
evening. Physical examination demonstrates right temporal artery distention and tenderness to touch over the right temporal region.
Laboratory evaluation reveals a significantly elevated erythrocyte sedimentation rate. Intravenous methylprednisolone is administered, and
her symptoms improve.

Two weeks later the patient returns to the emergency department reporting worsening jaw claudication and visual loss in the right eye.
Funduscopic examination is shown in the image below. Urgent treatment with intravenous tocilizumab and methylprednisolone is initiated.
Based on the vignette, which of the following are most likely inhibited by the pharmacologic management utilized in the treatment of this
patient?

⚪ A. Interleukin-6

⚪ B. Interleukin-10

⚪ C. Receptor activator of nuclear factor κB ligand

⚪ D. Transforming growth factor-β

⚪ E. ⍺4 integrin
 OUTLINE
1. T-cell Development
● A. Lymphoid Progenitor Cells

Immunology: ●
●
●
B. Precursor T-cell
C. Naïve T-cell Pre-selection
D. Positive Selection

T-cells ●
●
E. Negative Selection
F. Naïve T-cell Post-selection
2. Major Histocompatibility Complex
● A. MHC Class I
● B. MHC Class II
3. T-cell Activation
● A. Cytotoxic T-cell Activation
● B. Helper T-cell Activation
● C. Th1 Activation
● D. Th2 Activation
● E. Regulatory T-cell Activation
 Immunology: T-cells Bootcamp.com

• Lymphoid Progenitor Cells:

• Originate from the bone marrow
• Precursor T-cell:
• Leave bone marrow à Thymus
• CD4-/CD8-
• Naïve T-cell Pre-selection:
• TCR created using RAG1 and RAG2
• CD4+/CD8+
• Positive Selection:
• CD8+ binds with MHC I
• CD4+ binds with MHC II
• If binding is not adequate, naïve T-cell à Apoptosis
• Negative Selection:
• Self-antigens presented on MHC I and MHC II receptors
• If strong binding to self-peptides, naïve T-cell à Apoptosis
• Exception: T-regulatory cells (small percentage)
• AIRE protein (Autoimmune regulator protein)
• Naïve T-cell Post-selection (Immunocompetent):
• CD4+/CD8-, TCR à T-helper cell
• CD4-/CD8+, TCR à Cytotoxic T-cell
 Immunology: T-cells Bootcamp.com

• MHC Class I:
• Most nucleated cells • MHC Class II:
• Allows recognition of healthy vs infected cells • Antigen presenting cells
• HLA-A, HLA-B, HLA-C • HLA-DP, HLA-DQ, HLA-DR
• Receptor contains β2-microglobulin • Receptor has chains of equal length
• MHC I antigen complex developed in RER • Invariant chain prevents premature antigen binding
• Intracellular pathogens à CD8+ T-cells à Cell-mediated • Extracellular pathogens à CD4+ T-cells à Humoral
• Absence of MHC I à NK cell-mediated destruction
• Upregulated by IFN-⍺, IFN-β
 Immunology: T-cells Bootcamp.com

• Cytotoxic T-cell Activation: • Helper T-cell Activation:

• Nucleated cell presents Ag (endogenous) via MHC I • APC presents Ag via MHC II
• CD8+ T-cells bind to MHC I on nucleated cell • CD4+ T-cells bind to MHC II on APC
• Effective vs intracellular pathogens • B7-CD28 co-stimulatory signal
• Perforin, granzyme B released by CD8+ T-cell • Th1 Activation:
• Effective vs intracellular pathogens
• APC stimulates Th1 response via IL-12
• Th1 cells à IFN-ɣ, IL-2, TNF
• Granuloma formation
• Th2 Activation:
• Effective vs extracellular pathogens
• APC stimulates Th2 response via IL-4
• Th2 cells à IL-4, IL-5, IL-13

• Regulatory T-cell Activation:

• CD4+, CD25+, FOXP3+
• Protective vs self-antigens
• Prevent autoimmunity
• Stimulated by TGF-β, inhibited by IL-6
• Release TGF-β and IL-10 à ↓ Immune response
≣ Item 5 of 13 Test Your Knowledge
Difficulty Rating: ✪✪ Bootcamp.com
Question ID: 0062

A 10-month-old female presents with family to her pediatrician with a 4-day history of irritability and decreased appetite. Her mother reports
that her symptoms were accompanied by a fever that resolved yesterday. Shortly after the fever subsided, a generalized erythematous rash
on the trunk was noted by family. Since that time, the rash has spread to the face, neck, and lower extremities. Immunizations are current
and the family denies any recent illnesses or sick contacts. On examination the infant is well appearing with stable vital signs and a blanching
maculopapular rash extending from the trunk to the bilateral lower extremities.

CD56 positive lymphocytes in this patient most likely target infected cells through which process?

⚪ A. Interleukin-5 release

⚪ B. Interleukin-10 release

⚪ C. Absence of MHC I receptor

⚪ D. Presence of MHC II receptor

⚪ E. IL-4 release
 OUTLINE
1. B-cell Overview
● A. Lymphoid Progenitor Cells

Immunology: ●
●
●
B. Precursor B-cell
C. Naïve Mature B-cell
D. Proliferation

B-cells ● E. Plasma Cell

2. B-cell Activation
● A. Th-Dependent
● B. Th-Independent
● C. Affinity Maturation
● D. Isotype Switching
 Immunology: B-cells Bootcamp.com

• Lymphoid Progenitor Cells:

• Originate from the bone marrow
• Precursor B-cell:
• Stay in bone marrow to mature
• Naïve Mature B-cell:
• BCR: Membrane-bound IgM and IgD
• BCR generated from somatic recombination
• CD19, CD20, CD21
• MHC II receptor
• Proliferation:
• Lymphoid follicles à Germinal centers
• Plasma Cell:
• Produce and secrete antibodies
 Immunology: B-cells Bootcamp.com

• Th-Dependent:
• Peptide Ag
• T-cell activation via APC
• Naïve B-cell binds Ag to BCR
• B-cell receptor-mediated endocytosis of Ag
• Ag displayed on B-cell MHC II
• Activated Th-cell binds to B-cell
• CD40L-CD40 co-signal à Isotype class switching
• B-cell becomes activated à Proliferation à Plasma cell
• Th-Independent:
• Non-peptide conserved Ag
• Ex: Flagellin, LPS
• Cross-linking of surface IgG (BCR)
• Leads to production of IgM
• Affinity Maturation:
• B-cell à Lymph node à Secondary follicles
• Proliferation in germinal centers
• Random mutations of BCR à strongest affinity survives
• Isotype Switching:
• B-cell à Lymph node à Secondary follicles
• IL-4 à IgE, IgG
• IL-5 à IgA
• IL-13 à IgE
≣ Item 6 of 13 Test Your Knowledge
Difficulty Rating: ✪✪✪ Bootcamp.com
Question ID: 0063

A 32-year-old male with a past medical history of microscopic polyangiitis and end-stage renal disease presents to the emergency
department with a fever of 39.1 ℃ (102.4℉), abdominal pain, and general malaise over the past 6 hours. The patient states that he is on
home peritoneal dialysis and recently had his catheter replaced 5 days earlier without complication. Tenderness is noted over the abdomen
at the peritoneal catheter insertion site. The patient states his recently adopted dog playfully bit the insertion site of the dialysis tubing
causing a small puncture in the material just prior to symptom onset. Relevant laboratory studies are shown below. Intravenous antibiotics
are initiated. Blood cultures later grow Pasteurella multocida.

Hemoglobin: 11.1 g/dL

Leukocyte count: 3,200/mm3
Immunoglobulin M: 922 mg/dL (reference range: 40-345 mg/dL)
Immunoglobulin A: 88 mg/dL (reference range: 76-390 mg/dL)
Immunoglobulin G: 770 mg/dL (reference range: 650-1,500 mg/dL)

B-cells producing high quantities of immunoglobulin M in this patient are most likely responding to which antigen?

⚪ A. Lipoteichoic acid

⚪ B. Lipopolysaccharide

⚪ C. Exogenous bacterial peptide

⚪ D. Endogenous bacterial peptide

⚪ E. Host peptide
 OUTLINE
1. Antibody Structure
● A. Fc Region

Immunology: ● B. Fab Region

2. Antibody Properties
● A. V(D)J Recombination

Antibodies ●
●
●
B. Somatic Hypermutation
C. Affinity Maturation
D. Isotype Switching
● E. Primary Response
● F. Secondary Response
3. Immunoglobulin Isotypes
● A. IgM
● B. IgG
● C. IgA
● D. IgE
● E. IgD
 Immunology: Antibodies Bootcamp.com

• Fc Region:
• Consists of CH
• Determines isotype
• C-terminus
• Site of complement binding (IgM, IgG)
• Site of binding to phagocytes à Opsonization
• Carbohydrate side chains
• Fab Region:
• Consists of CL, VL, and VH
• Determines idiotype
• Binds antigens via epitope
 Immunology: Antibodies Bootcamp.com

• V(D)J Recombination:
• Heavy chain à VDJ
• Light chain à VJ
• Random recombination of genes à Fab
• Somatic Hypermutation à Affinity Maturation:
• Random variations of the variable region
• Activated B-cell à Lymph node à Secondary follicles
• Proliferation of B-cell in germinal centers
• Random mutations of BCR à Strongest affinity survives
• Isotype Switching:
• Activated B-cell à Lymph node à Secondary follicles
• Changes occur in CH domain (Fc)
• CD40-CD40L (B-cell – T-cell)
• IL-4 à IgE, IgG
• IL-5 à IgA
• IL-13 à IgE
• Primary Response:
• IgM initially released
• Secondary Response:
• Significantly larger IgG response
• IgM response is relatively unchanged
 Immunology: Antibodies Bootcamp.com

• IgM:
• Pentamer or monomer
• Pentamer linked by J-chain
• Early response to infection (vs IgG)
• Similar response on repeated exposure (vs IgG)
Monomer
• Activate complement IgD, IgE, IgG
• Acts as a BCR
• IgG:
• Most abundant immunoglobulin in blood
• Monomer
• Delayed response to infection (vs IgM)
• ↑↑ response on repeated exposure (vs IgM) Dimer
• Activate complement IgA
• Opsonization
• Acts as a BCR
• Passive immunity to fetus (from mother) via placenta
• IgA:
• Located primarily in MALT, breastmilk, sweat, saliva
• Monomer (circulation) à Dimer
• Dimer linked by J-chain
• Passive immunity to infant (from mother) via breastmilk
Pentamer
• IgE: IgM
• Monomer
• Fc binding to mast cell receptor à Crosslink allergen à degranulation
• Effective vs helminths à Eosinophils
• Type I Hypersensitivity reaction à Anaphylaxis
• IgD:
• Monomer
 Immunology: Antibodies Bootcamp.com

• Passive Immunity:
• Preformed antibodies
• Rapid, transient protective immunity
• Acquired from mother: IgG (placenta), IgA (breastmilk)
• Antivenom, Tetanus immunoglobulin
• Active Immunity
• Humoral response from pathogenic infection or external antigen
• Slow, long-lasting protective immunity
• Vaccination
≣ Item 7 of 13 Test Your Knowledge
Difficulty Rating: ✪✪✪ Bootcamp.com
Question ID: 0064

A researcher conducts an experiment to measure the effects of thymic tissue in adult mice. A control group and two additional groups of mice
are studied. Group 1 mice undergo a placebo surgical intervention, omitting thymectomy. Group 2 mice undergo surgical thymectomy. XX77,
a primary immunization is given 11 days prior to surgical intervention and a booster immunization is subsequently given 21 days later.

The data below is collected at 30 days after surgical intervention. Which of the following can the researcher most reasonably assume based
on the results of this experiment?

CD19+CD21+ XX77-specific heavy chain XX77-specific XX77-specific

(106 cells) variable region mutation IgM (µg/mL) IgG (µg/mL)
frequency

Control 24.3 4.7% 274 764

Group 1 21.1 2.1% 278 758

⚪ A. Impaired somatic hypermutation after surgery
Group 2 22.1 2.2% 271 767
⚪ B. Impaired isotype switching after thymectomy

⚪ C. Impaired V(D)J recombination after thymectomy

⚪ D. Marginal zone B-cell hyperplasia after surgery

⚪ E. Impaired CD40/CD40L binding after surgery

 OUTLINE
1. Complement Overview
● A. General Properties

Immunology: ● B. Functional Components

2. Complement Pathways
● A. Classical

Complement ●
●
●
B. Lectin
C. Alternative
D. Common
● E. Inhibitory
3. Disorders of Complement
● A. Early Complement Deficiency
● B. Terminal Complement Deficiency
● C. C1 Esterase Inhibitor Deficiency
● D. Paroxysmal Nocturnal Hemoglobinuria
 Immunology: Complement Bootcamp.com

• General Properties:
• Synthesized in liver (inactive state)
• Activation à Immunoglobulin, enzymes à C3b, MAC
• Inhibition à DAF (CD55), C1 esterase inhibitor
• Functional Components:
• C3a, C4aà ↑ Histamine release from mast cells à ↑ Vasodilation
• C5a à ↑ Neutrophil chemotaxis and ↑ Histamine release from mast cells à ↑ Vasodilation
• C3b à Opsonization
• C5b-9 Membrane Attack Complex (MAC) à Pathogen cell lysis
 Immunology: Complement Bootcamp.com

Functional Components of Complement

C3a, C4aà ↑ Histamine release from mast cells
C5a à ↑ Neutrophil chemotaxis and ↑ Histamine release from mast cells
• Classical: C3b à Opsonization
• Activation à IgM or IgG C5b-9 Membrane Attack Complex (MAC) à Pathogen cell lysis
• C1 complex à splits C4 and C2 à C4a, C4b, C2a, C2b
• C4b2b forms C3 convertase
• C4b2b3b forms C5 convertase
• Lectin:
• Activationà Mannose
• MBL binding to mannose forms C1-like complex
• C1-like complex à splits C4 and C2 à C4a, C4b, C2a, C2b
• C4b2b forms C3 convertase
• C4b2b3b forms C5 convertase
• Alternative:
• Activation à Microbial cell surface
• C3b bound to surface à binds factor B
• C3bBb forms C3 convertase
• C3b2Bb forms C5 convertase

• Common:
• C3 convertase à C3a (chemotaxis), C3b (C5 convertase formation)
• C5 convertase formation à C5a, C5b
• C5b à Binds C6-C9 à Forms MAC

• Inhibitory:
• C1-esterase inhibitor prevents cleavage of C2 and C4
• DAF (CD55) prevents formation of C3 convertase
• MIRL (CD59) prevents formation of MAC
 Immunology: Complement Bootcamp.com

• Early Complement Deficiency:

• Pathophysiology: Deficiency of C1-C4
• Presentation: Recurring respiratory/sinus infections
• ↑ Risk of developing SLE
• Terminal Complement Deficiency:
• Pathophysiology: Deficiency of C5-C9 (MAC)
• ↑ Risk of Neisseria sp. infections
• C1 Esterase Inhibitor Deficiency:
• Autosomal dominant
• Pathophysiology: ↑ Kallikrein à ↑ Bradykinin
• Presentation: Recurring angioedema (precipitated by trigger)
• Diagnostics: ↑ Bradykinin, ↓C4
• Avoid ACE inhibitors
• Paroxysmal Nocturnal Hemoglobinuria:
• Hemolytic anemia +/- pancytopenia
• Pathophysiology: Complement destruction of RBCs due to loss GPI proteins
• CD55/DAF and CD59/MIRL
• Presentation: Fatigue, pallor, intermittent jaundice, hemoglobinuria
• Venous thrombus in atypical locations à Budd-Chiari syndrome
• Diagnostics: Direct coombs negative
• Management: Eculizumab, Ravulozumab (Anti-C5 Ab)
≣ Item 8 of 13 Test Your Knowledge
Difficulty Rating: ✪✪✪ Bootcamp.com
Question ID: 0065

A 37-year-old female presents to the emergency department with a 3-day history of worsening severe left lower quadrant abdominal pain.
The patient states that she ordered a hamburger from a fast-food restaurant for dinner the day prior to onset of symptoms. The patient’s past
medical history includes allergies to dust, pollen, and numerous medications. Additionally, the patient was started on lisinopril by her primary
care physician one week prior for essential hypertension. Vital signs are stable. Physical examination reveals significant edema in the
bilateral upper extremities. When questioned regarding the swelling, the patient appears unconcerned and states “everyone in my family has
this happen from time to time.” Abdominal CT scan reveals significant diffuse bowel wall edema.

Which of the following sets of laboratory data are most consistent with this patient’s presentation?
Kallikrein Bradykinin Serum Serum C1-
C2 level C4 level inhibitor
function

⚪ A. A. ↑ ↑ ↑ ↑ ↑

⚪ B. B. ↑ ↑ ↑ ↑ ↓

⚪ C. C. ↓ ↓ ↑ ↑ ↑

⚪ D. D. ↓ ↑ ↑ ↑ ↓

⚪ E. E. ↑ ↑ ↑ ↓ ↓

⚪ F. F. ↑ ↑ ↓ ↓ ↓

⚪ G. G. ↑ ↑ ↓ ↓ ↑
 OUTLINE
1. Active vs Passive Immunity
● A. Active Immunity

Immunology: ● B. Passive Immunity

2. Vaccine Types
● A. Live Attenuated

Vaccinations ●
●
●
B. Whole Inactivated
C. Subunit Protein Inactivated
D. Subunit Polysaccharide Inactivated
● E. Subunit Polysaccharide + Conjugate Inactivated
● F. RNA
 Immunology: Vaccinations Bootcamp.com

• Active Immunity:
• Host generates Abs in immune response
• Delayed humoral response
• Repeated exposures à ↑ Ab response over time
• Natural à Infection
• Artificial à Immunization
• Passive Immunity:
• Preformed Abs administered
• Rapid humoral response
• t1/2 ~ 3 weeks à ↓ Ab response over time
• Natural à Mother IgG in fetal serum
• Artificial à Tetanus immunoglobulin (TIG)
 Immunology: Vaccinations Bootcamp.com

• Live Attenuated:
• Replicating live pathogen, less pathogenic, does not usually cause disease
• Compares to infectious immune response
• Avoided in immunocompromised (infants, elderly, pregnant, transplant, AIDS)
• Strong immune response à Humoral IgG and Cellular
• Less safe à Acquisition of virulence factor(s) à ↑ Pathogenicity
• Exception: Rotavirus vaccine
• Classic Examples: Varicella, MMR, Rotavirus, Yellow fever, Intranasal influenza, Oral polio (Sabin), BCG, Smallpox
• Whole Inactivated:
• Non-replicating, non-pathogenic virus/bacteria
• Moderate immune response à Humoral IgG
• Classic Examples: Influenza (IM), Hepatitis A, Polio (Salk), S. typhi (IM)
• Subunit Protein Inactivated:
• Antigenic (protein) components of pathogen
• Moderate immune response à Humoral IgG
• Classic Examples: Pertussis (acellular), Hepatitis B, HPV
• Toxoid vaccines use bacterial toxin à Tetanus, Diphtheria
• Subunit Polysaccharide Inactivated:
• Polysaccharide component of pathogen or Conjugate (polysaccharide + protein)
• Polysaccharide only à Th-Independent Response à Humoral IgM only
• Classic Example: PPSV23 (Strep pneumo)
• Subunit Polysaccharide + Conjugate Inactivated:
• Conjugate (polysaccharide + protein)
• Conjugate à Th-Dependent Response à Humoral IgG
• Classic Examples: PCV13 (Strep pneumo), Meningococcal, Hib
• RNA:
• mRNA à Ag production by host cells
• Classic Example: COVID-19
≣ Item 9 of 13 Test Your Knowledge
Difficulty Rating: ✪✪✪ Bootcamp.com
Question ID: 0066

A research group attempts to identify the effectiveness of “SSVK”, a vaccination against Shigella sonnei bacteria. Isolated S. sonnei were
grown in broth containing deoxycholate. Formalin was added to the vaccination sample for complete inactivation of pathogenicity. In pre-
clinical trials, the vaccine demonstrated immunogenicity against various strains of S. sonnei infected mice. Response per participant was
recorded as “strong” or “poor” utilizing cutoff serum values of specific immunoglobulins. Data collected is shown below.

Which of the following most likely describes the SSVK vaccine?

⚪ A. Live-attenuated
SSVK-specific SSVK-specific SSVK-specific SSVK-specific CD8+
serum IgG serum IgA fecal IgA Cytotoxic
⚪ B. Whole inactivated T-lymphocyte Assay

Strong 71 71 72 0
⚪ C. Subunit polysaccharide Response

Poor 2 2 1 73
⚪ D. DNA sequence Response

⚪ E. RNA sequence Total 73 73 73 73

Participants
 OUTLINE
1. B-cell and T-cell Variants
● A. Severe Combined Immunodeficiency

Immunology: ●
●
●
B. Bruton (X-linked) Agammaglobulinemia
C. Common Variable Immunodeficiency
D. Thymic Aplasia

Immunodeficiency 2.
●
Immunoglobulin Variants
A. Selective IgA Deficiency
● B. Hyper-IgM Syndrome
Syndromes ●
●
C. Hyper-IgE (Job) Syndrome
D. Wiskott-Aldrich Syndrome
3. Additional Variants
● A. IL-12 Receptor Deficiency
● B. Chronic Mucocutaneous Candidiasis
● C. IPEX Syndrome
 Immunology: Immunodeficiency Syndromes Bootcamp.com

• Severe Combined Immunodeficiency (SCID):

• Pathophysiology: Defective IL-2Rɣ receptor (MC mutation, XLR), Adenosine deaminase deficiency (AR), RAG mutations
• Presentation:
1. Normal newborn à Failure to thrive, recurring infections (thrush, diarrhea)
2. Absent lymphoid tissue (lymph nodes, tonsils)
• Diagnostics:
1. ↓ TRECs
2. Absent thymic shadow (CXR)
3. ↓↓↓ T-cells (Flow cytometry)
4. ↓↓↓ Serum Ig (all isotypes)
• Bruton (X-linked) Agammaglobulinemia:
• Pathophysiology: Defective BTK (XLR)
• Presentation:
1. Normal newborn à Failure to thrive, recurring infections (thrush, diarrhea)
2. Absent lymphoid tissue (lymph nodes, tonsils)
• Diagnostics:
1. ↓↓↓ B-cells [CD19, 20, 21] (Flow cytometry)
2. ↓↓↓ Serum Ig (all isotypes)
• Common Variable Immunodeficiency:
• Pathophysiology: Defective B-cell differentiation
• Presentation: Normal newborn à Recurring infections post-puberty
• Association: ↑ Risk of lymphoma and autoimmune disease
• Diagnostics: ↓ Ig (all types), plasma cells
• Thymic Aplasia:
• Pathophysiology: Defective 3rd and 4th pharyngeal pouch development à Thymic hypoplasia (or aplasia) à ↓↓↓ T-cells
• Presentation: DiGeorge à Hypocalcemia
• Association: ↑ Risk of lymphoma and autoimmune disease
• Diagnostics: ↓↓↓ T-cells (flow cytometry), ↓ PTH, ↓ Calcium, CXR: Absent thymus
 Immunology: Immunodeficiency Syndromes Bootcamp.com

• Selective IgA Deficiency:

• Pathophysiology: ↓↓↓ IgA
• Presentation: Less severe, respiratory illness, diarrhea (Giardia)
• Association:
1. Anaphylaxis with transfusion à Anti-IgA IgE
2. Celiac Disease (tTG-IgA à False negative)
• Diagnostics: ↓ Serum IgA, Normal IgM and IgG
• Hyper-IgM Syndrome:
• Pathophysiology: Defective CD40L (XLR)
• Presentation: Childhood opportunistic infections à Pneumocystis, Histoplasma, Cryptosporidium
• Diagnostics: Normal/↑ IgM, ↓↓↓ Serum IgA, IgG, IgE
• Hyper-IgE Syndrome (Job Syndrome):
• Pathophysiology: STAT3 mutation (AD) à ↓ Th17 à Impaired chemotaxis
• Presentation: Abscess without inflammation, coarse facies, eczema
• Diagnostics: ↑ IgE and eosinophils, ↓ IFN-ɣ
• Wiskott-Aldrich Syndrome
• Pathophysiology: WASp mutation (XLR) à Impaired antigen presentation
• Presentation: Eczema, purpura, encapsulated organism and opportunistic infections
• Association: ↑ Risk of lymphoma and leukemia
• Diagnostics:
1. ↑ IgA and IgE, Normal/↓ IgG and IgM
2. Thrombocytopenia (small platelets)
 Immunology: Immunodeficiency Syndromes Bootcamp.com

• IL-12 Receptor Deficiency:

• Pathophysiology: ↓ IL-12 receptor
• Presentation: Disseminated tuberculosis (Mycobacteria)
• Diagnostics: ↓IFN-ɣ
• Chronic Mucocutaneous Candidiasis:
• Pathophysiology: ↓ AIRE proteinà Defective IL-17/IL-17R à ↓ Response to Candida antigens
• Presentation: Recurring and/or refractory Candida infections
• Diagnostics: Absent cutaneous reaction to Candida antigens
• IPEX Syndrome:
• Pathophysiology: Mutation in FOXP3
• Presentation: Infancy
• Diagnostics: ↓↓↓ FOXP3, CD4+ CD25+ T-cells, Normal other T-cell lines
 Immunology: Immunodeficiency Syndromes Bootcamp.com

Disorder Pathophysiology Problem Classic Presentation Diagnostics Key Associations

SCID Defective IL-2R (XLR) Absent T-cells ↓ TRECs

ADA Deficiency (AR) +/- B-cell dysfunction Absent thymus
RAG mutation Normal newborn ↓↓↓ CD3+
Failure to thrive ↓↓↓ Serum Igs (all)
Recurring, opportunistic
Bruton Agammaglobulinemia Defective BTK gene (XLR) Absent mature B-cells infections ↓↓↓ CD19+, CD20+, CD21+
(Normal T-cells) ↓↓↓ Serum Igs (all)

CVID Defective B-cell differentiation Present dysfunctional B-cells Presents later (20-40y/o) ↓↓ Serum Igs (all) Lymphoma
(Normal T-cells) ↓↓ Plasma cells Autoimmune disease

Selective IgA Deficiency Anti-IgA antibodies ↓↓↓ IgA Respiratory illness ↓↓↓ IgA Celiac Disease
GI illness (Giardia) (False negative tTG-IgA)
Anaphylaxis to blood transx

Hyper IgM Syndrome Defective CD40L (XLR) Impaired class switching Childhood opportunistic -/↑ IgM
infections ↓↓↓ IgA, IgE, IgG

Hyper IgE Syndrome STAT3 mutation (AD) Impaired Abscess w/o inflammation ↑ IgE, eosinophils
neutrophil/macrophage Coarse facies ↓ IFN-ɣ
chemotaxis Eczema

Wiskott-Aldrich Syndrome WASp mutation (XLR) Impaired antigen presentation Purpura Thrombocytopenia Lymphoma
Eczema Unusually small platelets Leukemia
Recurring infections ↑ IgA, IgE
-/↓ IgM, IgG

IL-12R Deficiency ---- ↓ IL-12R Disseminated TB ↓ IFN-ɣ

Chronic Mucocutaneous ↓ AIRE protein à Defective Poor response to candida Ag Recurring/refractory candida Absent cutaneous rxn to Autoimmune disease
Candidiasis IL-17/IL-17R infections candida antigens

IPEX Syndrome Mutation in FOXP3 (X-linked) ↓ regulatory T-cells Enteropathy, dermatitis, ↓↓↓ FOXP3, CD4+ CD25+ Autoimmune disease
polyendocrinopathy Normal other T-cell lines Enteropathy
≣ Item 10 of 13 Test Your Knowledge
Difficulty Rating: ✪✪ Bootcamp.com
Question ID: 0067

A 21-year-old male presents to his primary care physician to establish care. He states that he has been suffering from rhinorrhea, intermittent
headaches, and cough for the past 2 weeks. He reports that this is his seventh illness this year and states that he recently recovered from a
prolonged course of watery diarrhea. He states that he has recently had multiple episodes of prolonged nose bleeds. Vaccinations are up to
date. The patient denies any sick contacts. Past medical and birth history are insignificant. Physical examination reveals increased nasal
mucus secretions and maxillary sinus pressure to percussion. Multiple ecchymoses are noted on the upper and lower extremities. The
patient is subsequently referred to a hematologist and immunologist for further evaluation. Diagnostic serum studies and flow cytometry
results are shown below. Lymph node biopsy reveals reactive follicular hyperplasia.

Which of the following immunologic disorders is most consistent with this patient’s presentation and diagnostic evaluation?

Hemoglobin: 16.1 g/dL

Leukocyte count: 8,200/mm3
Platelet count: 61,000/mm3
Prothrombin time: Normal
Partial thromboplastin time: Normal
Bleeding time: Prolonged
⚪ A. Common variable immunodeficiency Immunoglobulin A: 4 mg/dL (reference range: 76-390 mg/dL)
Immunoglobulin G: 37 mg/dL (reference range: 650-1500 mg/dL)
⚪ B. Acquired immunodeficiency syndrome Immunoglobulin M: 32 mg/dL (reference range: 50-170 mg/dL)
CD3+: 1,398 cells/mm3(reference range: 928-2,371 cells/mm3)
⚪ C. Interleukin-12 receptor deficiency CD3+CD4+: 770 cells/mm3(reference range: 501-1,401 cells/mm3)
CD19+ cells: 78 cells/mm3(reference range: 218-745 cells/mm3)
⚪ D. Severe combined immunodeficiency

⚪ E. X-linked agammaglobulinemia
 OUTLINE
1. Type I Hypersensitivity
● A. Classic Etiology

Immunology: ●
●
●
B. Early-Phase Mechanism
C. Late-Phase Mechanism
D. Presentation

Hypersensitivity ●
●
2.
E. Diagnostics
F. Non-IgE Mediated Histaminergic Reactions
Type II Hypersensitivity

Reactions ●
●
A. Destructive Mechanism
B. Receptor Binding Mechanism
● C. Diagnostics
3. Type III Hypersensitivity
● A. Mechanism
● B. Serum Sickness
● C. Serum Sickness-Like Reaction
● D. Arthus Reaction
4. Type IV Hypersensitivity
● A. Mechanism
● B. CD8+ Cytotoxicity
● C. Diagnostics
● D. Skin Differential
5. Summary Table
 Immunology: Hypersensitivity Reactions Bootcamp.com

• Classic Etiology:
• Foods (peanuts, shellfish)
• Medications (sulfa drugs)
• Insect sting
• Early-Phase Mechanism:
• Preformed IgE from previous sensitization
• IgE Fc portion bound to FcεRI on mast cells and basophils
• IgE Fab portion bound to antigen (allergen)
• Crosslinking à Degranulation à Histamine, tryptase release
• Bronchoconstriction, vasodilation, ↑ vascular permeability
• Late-Phase Mechanism:
• Prostaglandins, leukotrienes, and eosinophils à Inflammation
• Presentation:
• Mild: Bronchospasm, pruritis, urticaria, edema
• Severe: Anaphylaxis
• Diagnostics:
• Clinical in acute setting
• Serum tryptase
• Skin testing
• Non-IgE Mediated Histaminergic Reactions:
• Vancomycin à Rapid infusion
• Radioiodine contrast
• Low potency opioids
 Immunology: Hypersensitivity Reactions Bootcamp.com

• Destructive Mechanism:
• Cytotoxic Destruction Examples: AIHA, ITP, Acute hemolytic transfusion reaction, Erythroblastosis fetalis
• Inflammatory Examples: Goodpasture syndrome, Rheumatic fever, Hyperacute transplant rejection
• Ab binds to antigen on host cell surface (or graft)
1. MAC activated to destroy host cell
2. C3b à Opsonization à Phagocytosis of host cell
3. C5a à Neutrophil chemotaxis à Destruction of host cell
4. Antibody-dependent cell mediated cytotoxicity (NK cells)
• Receptor Binding Mechanism:
• Examples: Myasthenia gravis, Graves disease, Pemphigus vulgaris, Bullous pemphigoid
• Ab binds to receptor à Alteration of downstream signaling
• Myasthenia gravis à Blockade of AChR at NMJ
• Graves disease à Stimulation of TSHR
• Diagnostics:
• Direct Coombs Test: Tests for Ab bound to host cells
• Indirect Coombs Test: Tests for Ab present in host serum
 Immunology: Hypersensitivity Reactions Bootcamp.com

• Mechanism:
• Examples: Polyarteritis nodosa, PSGN, SLE, IgA nephropathy, Hypersensitivity pneumonitis
• Ag binds to IgG à Immune complex
• Deposited in tissues (Blood vessels, joints, kidney)
• Complement activation (↑↑↑ vs T2HS)
1. C3a, C4a, C5a à ↑ Vascular permeability à Edema
2. C5a à Neutrophil chemotaxis à Lysosomal destruction of tissue
• Vasculitis, arthritis, glomerulonephritis
• Serum Sickness:
• Etiology: Antitoxin/Antivenom, monoclonal antibodies
• Anti-Antivenom IgG created after initial exposure
• Re-exposure to Antivenom Ab à Immune complex formation (systemic)
• ↓ C3, C4 levels
• Serum Sickness-Like Reaction:
• Etiology: PCN, cephalosporins
• Not considered to be a Type III HS
• No immune complex formation
• Less systemic symptoms compared to Serum Sickness
• Normal complement levels
• Arthus Reaction
• Complication of vaccination (Tdap)
• Pre-sensitized host w/ preform antigen IgG
• Re-exposure via vaccine à Immune complex formation (local)
 Immunology: Hypersensitivity Reactions Bootcamp.com

• Mechanism:
• Examples: Allergic Contact Dermatitis
• Initial exposure to Ag/hapten
• APC presents Ag to naïve T-cells
• CD4+ T-cell binding to MHC II
• IL-12 stimulates Th1 differentiation
• IL-2, IFN-ɣ released by Th1 cells
• Re-exposure à Pre-formed T-cells
• ↑↑ IFN-ɣ released by Th1 cells
• Macrophage activation à Inflammatory response
• CD8+ T-cells target keratinocytes expressing Ag/hapten
• CD8+ Cytotoxicity:
• Examples: Multiple Sclerosis, IBD, T1DM, Hashimoto Thyroiditis
• CD8+ T-cell binding to MHC I
• Presenting cell lysis via perforins and granzymes
• Diagnostics:
• Tuberculin skin test
• Candida skin test
• Skin Differential:
• Allergic Contact Dermatitis à Poison Ivy (Urushiol), latex, nickel
• DRESS Syndrome à Allopurinol
• SJS/TEN à Lamotrigine, Phenytoin, Carbamazepine
Immunology: Hypersensitivity Reactions Bootcamp.com

Hypersensitivity Type Mechanism Presentation Diagnostics Key Components Key Examples

Type I Immediate Early phase: Urticaria, edema Serum tryptase IgE Food allergy
Mast cell and basophil Bronchospasm Skin testing Mast cells Insect stings
Preformed IgE Anaphylaxis Basophils
Crosslinks after Ag binding Eosinophils
Degranulation
Histamine release

Late Phase:
Prostaglandins, Leukotrienes
Eosinophils

Type II Cytotoxic Ab bind to host cell surface Variable depending on AIHA, ITP
Ag binds to Ab cells destroyed Acute hemolytic reaction
MAC-induced cytolysis (i.e., AIHA, RBCs) Erythroblastosis fetalis
Direct Coombs Test
C3b-induced opsonization Indirect Coombs Test IgG and/or IgM
Type II Inflammatory C5a-induced chemotaxis Complement Goodpasture syndrome
Serum antibody
NK ADCC Neutrophils Rheumatic fever •
Natural killer cells Hyperacute transplant rej.
•
Type II Receptor Binding Ab binds to receptor Variable depending on Myasthenia gravis •
Downstream signaling receptor Graves’ Disease •
Type III Immune Complex Ag-Ab immune complex Vasculitis ↓ Serum C3, C4 IgG Polyarteritis nodosa •
Deposits in tissues Arthritis Complement PSGN •
C3a, C4a, C5a à Edema Glomerulonephritis Neutrophils SLE •
C5a-induced chemotaxis (among others) Serum sickness •
Arthus reaction •
Type IV Delayed (Cell-mediated) APCà Ag to CD4+ T-cell Variable depending on Tuberculin skin test CD4+ T-cells Allergic contact dermatitis
IL-12 stimulates Th1 tissue and cells destroyed Candida skin test CD8+ T-cells Multiple Sclerosis
IL-2, IFN-ɣ release by Th1 (i.e., T1DM, pancreas) Neutrophils, Macrophages Inflammatory Bowel Disease
Type 1 Diabetes Mellitus
MHC Ià Ag to CD8+ T-cell Hashimoto Thyroidtis
Destruction of host cell
≣ Item 11 of 13 Test Your Knowledge
Difficulty Rating: ✪✪ Bootcamp.com
Question ID: 0068

A 44-year-old African American female with a past medical history of childhood asthma presents to the emergency department with
worsening dyspnea over the past 4 days. She states that she was initially treated for a presumed asthma exacerbation with oral steroid
medication. She also reports difficulty sleeping at night due to night sweats and worsening anxiety. She has approximately 9.1kg (20 lbs) of
unintentional weight loss over the past month. Additionally, she reports cramping, non-specific abdominal and diffuse joint pain that started
insidiously months earlier. Chest computed tomography imaging reveals a large left lower lobe mass and significant hilar lymphadenopathy.
Subsequent biopsy of the hilar lymph node is conducted and shown below. Bronchoscopy revealed granulomatous inflammation without
evidence of malignancy or infectious etiology. A regimen of high-dose prednisone is initiated.

Which of the following best describes the mechanism of this patient’s underlying disease?

⚪ A. Fc-receptor mediated immune cell activation

⚪ B. IgG mediated inhibition of signaling pathways

⚪ C. IgE mediated mast cell degranulation

⚪ D. Th1-cell mediated interferon-gamma release

⚪ E. Deposition of antigen-antibody complexes

 OUTLINE

1. Acute Hemolytic Reaction 4. TRALI

● A. Classic Etiology ● A. Classic Etiology

Immunology: ●
●
B. Mechanism
C. Presentation
●
●
B. Mechanism
C. Presentation

Transfusion
● D. Diagnostics ● D. Diagnostics
● E. Management ● E. Management
2. Delayed Hemolytic Reaction 5. Anaphylactic Reaction

Reactions
● A. Classic Etiology ● A. Classic Etiology
● B. Mechanism ● B. Mechanism
● C. Presentation ● C. Presentation
● D. Diagnostics ● D. Diagnostics
● E. Management ● E. Management
3. Febrile Non-hemolytic Reaction
● A. Classic Etiology
● B. Mechanism
● C. Presentation
● D. Diagnostics
● E. Management
 Immunology: Transfusion Reactions Bootcamp.com

• Classic Etiology:
• Incompatibility RBC antigens (ABO)
• Mechanism:
• Destruction of donor RBCs by recipient preformed Abs (RBC transfusion)
• Destruction of recipient RBCs by donor preformed Abs (FFP transfusion)
• Type II hypersensitivity
• During or hours after transfusion
• Presentation:
• Symptoms of hemolysis: Jaundice, chills, hemoglobinuria
• Pain at IV site
• Hypotension, tachycardia
• Diagnostics:
• Positive Direct Coombs Test
• ↑ LDH, ↑ bilirubin, ↓ haptoglobin
• Management:
• Stop transfusion

Red Blood Fresh Frozen

Cell Txn Plasma Txn

Universal Type O Type AB

Donor

Universal Type AB Type O

Recipient
 Immunology: Transfusion Reactions Bootcamp.com

• Classic Etiology:
• Incompatibility RBC antigens (Kidd, D)
• Mechanism:
• Destruction of donor RBCs by recipient preformed Abs (RBC transfusion)
• Anamnestic response
• Type II hypersensitivity
• Weeks or months after transfusion
• Presentation:
• Mild symptoms
• Classic presentation: Recurring blood transfusions
• Diagnostics:
• Positive Direct Coombs Test
• ↑ LDH, bilirubin, ↓ haptoglobin
• Management:
• Self-limited
• Transfusion generally completed at time of reaction
 Immunology: Transfusion Reactions Bootcamp.com

• Classic Etiology:
• Donor WBC cytokines and antigens
• Mechanism:
• WBC cytokines leak
• Donor WBCs targeted by recipient preformed antibodies
• During or hours after transfusion
• Presentation:
• Generally, milder than acute hemolytic reaction
• Classic vignette: Pediatric patient
• Diagnostics:
• Negative Direct Coombs Test
• Normal LDH, bilirubin, haptoglobin
• Management:
• Stop transfusion
• Future occurrences à Leukoreduced blood products
 Immunology: Transfusion Reactions Bootcamp.com

• Classic Etiology:
• Neutrophil and/or pulmonary endothelial activation
• Mechanism:
• ↑ Neutrophil priming and activation à Proinflammatory cytokine release
• ↑ Pulmonary vascular permeability
• Pulmonary edema (Noncardiogenic)
• During or hours after transfusion
• Presentation:
• Dyspnea
• Classic vignette: FFP or platelet transfusion
• Diagnostics:
• Interstitial infiltrates on CXR (transient)
• Negative Direct Coombs Test
• Normal LDH, bilirubin, haptoglobin
• Management:
• Stop transfusion
• Respiratory support à O2 supplementation, intubation
• Resolves spontaneously
 Immunology: Transfusion Reactions Bootcamp.com

• Classic Etiology:
• Recipient IgA deficiency
• Mechanism:
• Recipient has preformed anti-IgA IgE antibodies on mast cells
• Donor IgA in blood sample
• IgE-mediated degranulation à Histamine
• Type I hypersensitivity
• During or hours after transfusion
• Presentation:
• Hypotension, tachycardia
• Wheezing, urticaria
• Diagnostics:
• Negative Direct Coombs Test
• Normal LDH, bilirubin, haptoglobin
• Management:
• Stop transfusion à Epinephrine
• Respiratory support
• Future occurrences à IgA deficient blood products
 Immunology: Transfusion Reactions Bootcamp.com

Transfusion Reaction Mechanism Presentation Diagnostics Management Key Vignette Associations

Acute Hemolytic Reaction Donor RBC destroyed Symptoms of Positive Direct Coombs Type and screen ABO incompatibility
Recipient Abs hemolysis ↑ LDH, ↑ bilirubin
Type II HS Pain at IV site ↓ Haptoglobin
During (or hours after) Hypotension
Tachycardia

Delayed Hemolytic Reaction Donor RBC destroyed Mild symptoms Positive Direct Coombs Self-limited Frequent blood transfusions
Recipient Abs ↑ LDH, ↑ bilirubin IVDU
Anamnestic response ↓ Haptoglobin
Type II HS

Immediate cessation of transfusion

Weeks (or months) after

Febrile Non-hemolytic Donor WBC cytokine Mild symptoms Negative Direct Coombs Leukoreduced blood Pediatric patient
Reaction leak Normal LDH, bilirubin
Recipient Abs Normal haptoglobin
Hours after (or during)

Transfusion Related Acute ↑ Neutrophil priming and Dyspnea Negative Direct Coombs Respiratory support FFP or platelet transfusion
Lung Injury (TRALI) activation Increasing O2 req. Normal LDH, bilirubin Resolves spontaneously
↑ Pulmonary vascular Normal haptoglobin
permeability
Pulmonary edema
Hours after (or during)

Anaphylactic Reaction Donor IgA Urticaria Negative Direct Coombs Respiratory support IgA deficiency
Recipient anti-IgA IgE Wheezing Normal LDH, bilirubin IgA-deficient blood
Mast cell degranulation Hypotension Normal haptoglobin
Type I HS Tachycardia
During (or hours after)
 OUTLINE

1. Transplantation Principles 5. Graft vs Host Disease

● A. Transplant Terminology ● A. Classic Etiology

Immunology: ●
●
B. Graft Terminology
C. Human Leukocyte Antigen
●
●
B. Mechanism
C. Presentation

Transplant
2. Hyperacute Rejection ● D. Histopathology
● A. Classic Etiology ● E. Management
● B. Mechanism ● F. Additional Considerations

Rejection
● C. Presentation 6. Transplant Rejection Summary
● D. Histopathology 7. Immunosuppressants
● E. Management ● A. Calcineurin Inhibitors
3. Acute Rejection ● B. mTOR Inhibitors
● A. Classic Etiology ● C. IL-2 Receptor Inhibitors
● B. Mechanism ● D. Recombinant IL-2
● C. Presentation ● E. Glucocorticoids
● D. Histopathology ● F. Purine Inhibitors
● E. Management 8. Biologic Immunotherapy
4. Chronic Rejection ● A. TNF-Inhibitors
● A. Classic Etiology ● B. Monoclonal Antibodies
● B. Mechanism
● C. Presentation
● D. Histopathology
● E. Management
 Immunology: Transplant Rejection Bootcamp.com

• Transplant Terminology:
• Autologous: Donor to self
• Isotransplantation: Donor to genetically identical recipient
• Allogeneic: Donor to another non-genetically identical recipient
• Graft Terminology:
• Autograft: Donor graft to self
• Isograft: Donor graft to genetically identical recipient
• Allograft: Donor graft to non-genetically identical recipient
• Xenograft: Donor graft to different species recipient
• Human Leukocyte Antigen:
• HLA gene cluster codes for MHC
• HLA-A, HLA-B, HLA-C: Codes for MHC I
• HLA-DR, HLA-DP, HLA-DQ: Codes for MHC II
 Immunology: Transplant Rejection Bootcamp.com

• Classic Etiology:
• RBC major antigen (ABO) incompatibility
• HLA incompatibility
• Mechanism:
• Destruction of donor graft by recipient preformed Abs
• Type II hypersensitivity
• Onset within minutes of graft placement
• Presentation:
• Immediate edema to graft tissues
• Histopathology:
• Thrombosis and fibrinoid necrosis of small vessels
• Necrosis of graft
• Management and Preventative:
• Remove graft
• Cross matching major RBC (ABO) antigens
• HLA matching
 Immunology: Transplant Rejection Bootcamp.com

• Classic Etiology:
• HLA incompatibility
• Mechanism:
• Primarily cell-mediated or humoral rejection only
• Cell-mediated response (Type IV hypersensitivity) à Macrophage and CD8+ T-cell activation à Cytotoxicity to graft
• Humoral response (Type II hypersensitivity) à Antibody production à Complement-mediated destruction of graft
• Onset weeks-months
• Presentation:
• Edema to graft tissues
• Deterioration of transplanted tissue function
• Histopathology:
• Lymphocytic infiltrate (Cell-mediated)
• Vasculitis
• Complement marker + à Consider humoral rejection
• Complement marker - à Consider cell-mediated rejection
• Management and Prevention:
• HLA matching
• Immunosuppression
 Immunology: Transplant Rejection Bootcamp.com

• Classic Etiology:
• HLA incompatibility
• Mechanism:
• Cell-mediated and humoral rejection integrated together
• Cell-mediated response (Type IV hypersensitivity) à Macrophage and CD8+ T-cell activation à Cytotoxicity to graft
• Humoral response (Type II hypersensitivity) à Antibody production à Complement-mediated destruction of graft
• Onset months-years
• Presentation:
• Edema to graft tissues
• Deterioration of transplanted tissue function
• Histopathology:
• Arteriosclerosis
• Interstitial fibrosis
• Vascular smooth muscle proliferation
• Atrophic graft tissues
• Management and Prevention:
• Remove graft
• Immunosuppression
 Immunology: Transplant Rejection Bootcamp.com

• Classic Etiology:
• Hematopoietic stem cell transplantation
• Liver transplantation
• Mechanism:
• Donor T-cells à Cell-mediated response à Host tissue damage
• Type IV hypersensitivity
• Onset variable
• Presentation:
• Dermatologic à Maculopapular rash
• Hepatobiliary à Jaundice, ↑ ALP
• Intestinal à Non-specific abdominal pain, nausea, emesis, diarrhea
• Hematologic à Pancytopenia
• Histopathology:
• Lymphocytic infiltration of host specimen
• Management and Prevention:
• Immunosuppression
• Additional Consideration:
• Graft vs tumor effect
Immunology: Transplant Rejection Bootcamp.com

Rejection Type Classic Onset Cell-Mediated Mechanism Presentation Histopathology

Humoral

Hyperacute Minutes Humoral Donor graft destruction Immediate edema to graft Thrombosis
Recipient pre-formed Abs tissues Fibrinoid necrosis
Type II HS Necrosis of graft

Acute Weeks to months Cell-mediated CM: Recipient T-cell activation Edema to graft tissues Lymphocytic infiltrate
Or Type IV HS Vasculitis
Humoral ↓ Function of transplanted
H: Recipient Ab production vs graft tissues
Chronic Months to years Cell-mediated Type II HS Interstitial fibrosis
And Vascular smooth muscle proliferation
Humoral Atrophic graft tissues

Graft vs Host Variable Cell-mediated Donor T-cell activation Maculopapular rash Lymphocytic infiltrate on host specimen (e.g.,
Type IV HS Jaundice, scleral icterus skin)
Abdominal pain
Pancytopenia
 Immunology: Transplant Rejection Bootcamp.com

• Drug Class: Calcineurin Inhibitors

• Examples: Cyclosporine, Tacrolimus
• Cyclosporine Mechanism: Binds cyclophilin à ↓ IL-2
• Tacrolimus Mechanism: Binds FK506BP à ↓ IL-2
• HY Indications: Transplant rejection prophylaxis, psoriasis
• HY Adverse Effects: Nephrotoxicity, neurotoxicity
• Cyclosporine Specifics à Gingival hyperplasia, hirsutism

• Drug Class: mTOR Inhibitor

• Examples: Sirolimus (Rapamycin)
• Mechanism: Binds FKBP
• HY Indications: Transplant rejection prophylaxis (Renal)
• HY Adverse Effects: Pancytopenia
• No nephrotoxicity

• Drug Class: IL-2R Inhibitor

• Examples: Basiliximab, Daclizumab
• Mechanism: Blocks IL-2R receptor
• HY Indications: Transplant rejection prophylaxis (Renal)
• HY Adverse Effects: Hypertension, edema
• Type II hypersensitivity

• Drug Class: Recombinant IL-2

• Examples: Aldesleukin
• Mechanism: Activates lymphoid cells vs malignancy
• HY Indications: Renal cell carcinoma, metastatic melanoma
 Immunology: Transplant Rejection Bootcamp.com

• Drug Class: Glucocorticoids

• Examples: Prednisone, Dexamethasone, Methylprednisolone
• Mechanism: Inhibit NF-κB and inflammatory cytokine genes
• HY Indications: AI, asthma, acute inflammatory states
• HY Adverse Effects: Osteoporosis, Cushing syndrome,
• HY Adverse Effects: Hyperglycemia, amenorrhea
• Additional: Leukocytosis, iatrogenic AI with abrupt discontinuation
• Avascular necrosis of femoral head

Drug Class: Purine Inhibitors

• Examples: Azathioprine (6-MP), Mycophenolate, Ribavirin, MTX
• Azathioprine: Indirectly cytotoxic to PRPP Amidotransferase
• Mycophenolate: Reversible inhibition of IMPDH
• Methotrexate (MTX): Inhibits dihydrofolate reductase
• HY Indications: Rheumatoid arthritis
• HY Adverse Effects: Pancytopenia
• Additional: ↑↑ 6-MP w/ allopurinol
• Additional: Mycophenolate à Invasive CMV
 Immunology: Transplant Rejection Bootcamp.com

• Drug Class: TNF-inhibitors

• Examples: Infliximab, Adalimumab, Golimumab, Certolizumab
Monoclonal Ab Target HY Indication HY Adverse Effect • Infliximab: Chimeric anti-TNF Ab
• Adalimumab, Golimumab, Certolizumab: Humanized anti-TNF Ab
• Etanercept: Fusion protein for TNF + IgG1 Fc
Natalizumab ⍺4-integrin Multiple sclerosis Reactivation of JC virus
• HY Adverse Effects: Tuberculosis (Screen prior to administration)
Rituximab CD20 Many diseases Reactivation of JC virus

Palivizumab RSV F protein RSV prophylaxis --

Omalizumab Soluble IgE Severe/refractory allergic --

asthma

Trastuzumab HER2/neu HER2/neu + breast ca Dilated cardiomyopathy

Eculizumab C5 PNH Encapsulated bacterial

infections

Bevacizumab VEGF Many cancers GI bleeding

Cetuximab EGFR inhibitor Many cancers --

Panitumumab

Denosumab RANKL Osteoporosis Hypocalcemia

Pembrolizumab PD-1 Many cancers

Abciximab GP IIb/IIIa receptor PCI Bleeding

Alemtuzumab CD52 CLL ITP

Ustekinumab IL-12, IL-23 Psoriasis

Ipilimumab CTLA-4 Many cancers

 Immunology: Lymphoid Tissue Bootcamp.com

• Thymus.JPG
• https://commons.wikimedia.org/wiki/File:Thymus.JPG
• Tourbulence at Dutch WikipediaLater versions were uploaded by Siebrand at nl.wikipedia., CC BY-SA 3.0 <http://
creativecommons.org/licenses/by-sa/3.0/>, via Wikimedia Commons
• X-ray of an infant with a prominent thymus
• https://commons.wikimedia.org/wiki/File:X-ray_of_an_infant_with_a_prominent_thymus.jpg
• Nausheen Khan, Dimakatso C. Thebe, Farhanah Suleman, Irma van de Werke, CC BY 4.0
<https://creativecommons.org/licenses/by/4.0>, via Wikimedia Commons
• Thymic corpuscle
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• Lymphatic immune system lymphnode5-CROPPED
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• Progressive transformation of germinal centres -1- very low mag
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_very_low_mag.jpg
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• Peyer’s patch (improved color)
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 Immunology: Innate vs Adaptive Immunity Bootcamp.com

• 20100825 023736 Neutrophil

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• Bob Blaylock, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons
• Hem1Eosinophile
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• Hem1Basophile
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• El*Falaf, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons
• Monocytes, a type of white blood cell (Giemsa stained)
• https://commons.wikimedia.org/wiki/File:Monocytes,_a_type_of_white_blood_cell_(Giemsa_stained).jpg
• Dr Graham Beards, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons
 Immunology: Inflammation Bootcamp.com

• TLR Signaling Pathway

• Adapted from “TLR Signaling Pathway”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-templates
• Leukocyte Migration at Sites of Infection
• Adapted from “Leukocyte Migration at Sites of Infection”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-templates
• Neutrophil
• Adapted from “Endothelial Barrier Inflammation and Leak (Layout)”, by BioRender.com (2021). Retrieved from
https://app.biorender.com/biorender-templates
• Leukocyte Adhesion Deficiency
• Adapted from “Leukocyte Migration at Sites of Infection”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-templates
• Granuloma
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• Granulomatous Inflammation Mechanism
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• Necrogran10x
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• Granuloma mac
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• Sanjay Mukhopadhyay, Public domain, via Wikimedia Commons
 Immunology: Cytokines Bootcamp.com

• Cytokines
• Adapted from “Induction of 2nd Order Cytokines”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-templates
• T-cell Lines
• Adapted from “T cell activation and differentiation”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-templates
 Immunology: T-cells Bootcamp.com

• Thymus T-Cell Development

• Adapted from “T-Cell Development in Thymus 2”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-templates
• MHC Class 1.svg
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• MHC Class 2.svg
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• Macrophage Activation via MHC II
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• T-cell Activation, CD8+
• Created with BioRender.com
• T-cell Activation, CD4+
• Created with BioRender.com
 Immunology: B-cells Bootcamp.com

• B-cell
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• Figure 42 02 06.jpg
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• Steps in B-cell Differentiation
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• Lymph Node
• Created with BioRender.com
 Immunology: Antibodies Bootcamp.com

• Antibody Structure
• Adapted from “The Variable Region of an Antibody Binds to the Antigen”, by BioRender.com (2021). Retrieved from
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• Mono-und-Polymere.svg
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 Immunology: Complement Bootcamp.com

• Three Pathways of Complement Activation

• Adapted from “Three Pathways of Complement Activation”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-
templates
 Immunology: Vaccinations Bootcamp.com

• Three Pathways of Complement Activation

• Adapted from “Three Pathways of Complement Activation”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-
templates
 Immunology: Immunodeficiency Syndromes Bootcamp.com

• CD40 Ligand Deficiency

• Adapted from “CD40 Ligand Deficiency”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-templates
• T-cell Activation, CD4+
• Created with BioRender.com
• Candida antigen test
• Adapted from “Candida antigen test”, by BioRender.com (2021). Retrieved from https://app.biorender.com/biorender-templates
 Immunology: Hypersensitivity Reactions Bootcamp.com

• Type I Hypersensitivity Reaction Mechanism

• Created with BioRender.com
• EMminor2010.JPG
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• James Heilman, MD, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons
• Type II Hypersensitivity Reaction Mechanism
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• Myasthenia MOA
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Retrieved from https://app.biorender.com/biorender-templates
• Graves Disease MOA
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• Type III Hypersensitivity Reaction Mechanism
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• Churg-Strauss syndrome – high mag.jpg
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• Churg-Strauss syndrome – very high mag.jpg
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• Type IV Hypersensitivity Reaction Mechanism
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• Poison ivy contact dermatitis.jpg
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 Immunology: Transfusion Reactions Bootcamp.com

• ABO blood type.svg

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• Blood-centrifugation-scheme.png
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• RBC Transfusion Reaction
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• Leukocyte Cytokines
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• Transfusion-related acute lung injury chest X-ray.gif
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• Altaf Gauhar Haji, Shekhar Sharma, DK Vijaykumar and Jerry Paul., CC BY 2.0 <https://creativecommons.org/licenses/by/2.0>, via
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• IgA Deficiency Transfusion
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 Immunology: Transplant Rejection Bootcamp.com

• Lung transplant rejection – high mag.jpg

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• Nephron, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons
• Glucocorticoid Pathway
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• Calcineurin Inhibitor and mTOR inhibitor Pathway
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