Immunology

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Immunology — Key Facts for NEET PG

• Innate Immunity: First line — physical barriers, phagocytes (neutrophils, macrophages), NK cells, complement; No memory
• Adaptive Immunity: Second line — T cells (cell-mediated) + B cells (humoral); Memory; Clonal expansion; Specific
• Antibodies (Ig): IgG (most abundant, crosses placenta), IgM (first response, pentamer), IgA (mucosal), IgE (allergy, parasites), IgD (surface on B cells)
• MHC/HLA: Class I (all nucleated cells, CD8), Class II (APC — dendritic, macrophage, B, CD4)
• ⚡ Exam tip: Type I hypersensitivity = IgE-mediated (anaphylaxis, allergies); Type IV = T-cell mediated (TB skin test, contact dermatitis) — delayed

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🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

Immunology — NEET PG Study Guide

Cells of the Immune System

Phagocytes:

• Neutrophils: First responders, bacterial infections, PMNs with multilobed nucleus
• Macrophages: Tissue-resident, phagocytosis, antigen presentation
• Dendritic Cells: Best antigen-presenting cells (APCs), link innate and adaptive

Lymphocytes:

• T cells: Cell-mediated immunity (65-70% of lymphocytes)
  • CD4+ helper T cells (Th1, Th2, Th17, Tfh, Treg)
  • CD8+ cytotoxic T cells
• B cells: Humoral immunity (10-15%), produce antibodies
• NK cells: Innate lymphoid cells, kill virus-infected and tumor cells (no prior sensitization)

Antibody Structure

Basic Y-shape:

• 2 heavy chains + 2 light chains
• Variable regions (antigen binding)
• Constant regions (effector functions)
• Fab fragment: Antigen binding
• Fc fragment: Effector functions (complement activation, Fc receptor binding)

Types of Immunity

Active Immunity: Host produces antibodies; Long-lasting; Takes time to develop

• Natural: Infection
• Artificial: Vaccination

Passive Immunity: Receive antibodies; Immediate; Short-lived

• Natural: Maternal IgG crosses placenta, IgA in breast milk
• Artificial: Antiserum, immunoglobulin

NCE Exam Pattern

Common question types:

1. Innate vs adaptive immunity
2. Antibody classes and functions
3. T cell subsets and functions
4. Antigen presentation and MHC
5. Hypersensitivity reactions

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🔴 Extended — Deep Study (3mo+)

Comprehensive coverage for students on a longer study timeline.

Immunology — Comprehensive NEET PG Notes

Detailed Theory

1. Innate Immunity

Physical Barriers:

• Skin: Keratinized epithelium
• Mucous membranes: Respiratory, GI, GU tracts
• Cilia: Respiratory epithelium (mucociliary escalator)
• Gastric acid, lysozyme, defensins

Cellular Defenses:

Neutrophils:

• Most abundant WBC (40-70%)
• Phagocytose bacteria
• PMNs: 2-5 lobes
• Burst (respiratory burst): ↑ NADPH oxidase → superoxide → reactive oxygen species

Macrophages:

• Tissue-resident (Kupffer cells in liver, microglia in brain)
• M1 (classical activation): Pro-inflammatory, kills microbes, Th1 response
• M2 (alternative activation): Anti-inflammatory, wound healing
• Important in granuloma formation

Dendritic Cells:

• Best APCs for naive T cells
• Capture antigen in periphery, migrate to lymph nodes
• Express high MHC II

NK Cells:

• Kill cells with decreased MHC I (virus-infected, tumor)
• “Missing self” recognition
• NKG2D recognizes stress-induced ligands
• KIRs (Killer Immunoglobulin-like Receptors) regulate activity

Eosinophils:

• Defend against parasites
• Major basic protein, eosinophil cationic protein
• High-affinity IgE receptors

Basophils/Mast Cells:

• IgE-mediated reactions
• Histamine, heparin, leukotrienes
• Anaphylaxis, allergic diseases

2. Complement System

Pathways:

• Classical: C1q binding to antibody (IgG/IgM) complexes
• Alternative: Spontaneous C3 hydrolysis, properdin stabilization
• Lectin: Mannose-binding lectin (MBL) binding to mannose on pathogens

All pathways converge at C3 convertase → C3 → C5 convertase → C5 → MAC

Biological Functions (MAC — Membrane Attack Complex):

• C5b6789 → Forms pore in target membrane
• Lysis of Gram-negative bacteria
• Opsonization (C3b)
• Inflammation (C3a, C5a — anaphylatoxins)

Complement Regulation:

• C1 inhibitor (C1INH): Prevents C1 activation
• Decay-accelerating factor (DAF/CD55): Accelerates C3 convertase decay
• Factor H, Factor I: Alternative pathway regulators

Deficiencies:

• C1, C2, C4: SLE-like disease (impaired immune complex clearance)
• C3: Severe recurrent infections
• C5-9: Neisserial infections (MAC deficiency)

3. Adaptive Immunity — T Cells

T Cell Development:

• In thymus
• Positive selection (survival of T cells that recognize self-MHC)
• Negative selection (deletion of self-reactive T cells)
• TCR (T cell receptor): αβ (most) or γδ chains

CD4+ Helper T Cells:

• MHC II restricted
• Helper T cells — “orchestrate” immune response
• Th1: IFN-γ, activate macrophages, fight intracellular pathogens
• Th2: IL-4, IL-5, IL-13, help B cells, fight parasites, allergy
• Th17: IL-17, IL-22, neutrophil recruitment, extracellular bacteria, autoimmunity
• Tfh: B cell help in germinal centers
• Treg: Suppress immune responses (FOXP3)

CD8+ Cytotoxic T Cells:

• MHC I restricted
• Kill virus-infected cells, tumor cells
• Perforin + Granzyme pathway
• Fas-FasL pathway
• Memory CD8+ T cells persist

T Cell Activation:

1. TCR recognizes antigen presented on MHC
2. Co-stimulation (CD28 on T cell binds B7 on APC)
3. Cytokines determine differentiation
4. Clonal expansion

4. Adaptive Immunity — B Cells

B Cell Development:

• In bone marrow
• Heavy chain gene rearrangement first
• Light chain rearrangement
• Surface IgM as BCR
• Negative selection (self-reactive B cells eliminated)

B Cell Activation:

1. Antigen binds BCR (native antigen)
2. Internalization, processing, presentation on MHC II
3. Th cell help (CD40L-CD40, cytokines)
4. Clonal expansion
5. Differentiation to plasma cells (antibody factories) and memory B cells

Antibody Production:

• Primary response: IgM first, then IgG (class switching)
• Secondary response: Faster, stronger, mostly IgG (memory)

5. Immunoglobulins — Detailed

IgG:

• Most abundant (75-80%)
• Crosses placenta (only Ig to cross)
• Opsonization, complement activation (classical)
• Neutralization, ADCC
• Long half-life
• 4 subclasses (IgG1, IgG2, IgG3, IgG4)

IgM:

• Pentamer (5 Y-shaped units)
• First antibody produced in infection
• Strong complement activator
• Does not cross placenta
• ABO blood group antibodies

IgA:

• Dimer (in secretions), monomer (serum)
• Most produced Ig daily
• Secretory component protects from degradation
• Mucosal immunity (saliva, tears, breast milk, respiratory/GI/GU secretions)

IgE:

• Least abundant
• Bound to mast cells/basophils via FcεRI
• Immediate hypersensitivity (anaphylaxis, allergies)
• Defense against parasites
• Allergen-specific IgE in atopy

IgD:

• Low serum levels
• Co-expressed with IgM on naive B cells (B cell function unclear)

6. Antigen Presentation

MHC Class I:

• On all nucleated cells
• Presents endogenous antigens (cytoplasmic — viral, tumor)
• Binds CD8+ T cells
• β2-microglobulin associated
• Peptides: 8-10 amino acids

MHC Class II:

• On professional APCs (dendritic, macrophage, B cells)
• Presents exogenous antigens (phagocytosed)
• Binds CD4+ T cells
• Invariant chain (Ii) blocks binding in ER
• CLIP peptide exchange with antigen

Cross-Presentation:

• Dendritic cells present exogenous antigens on MHC I
• Important for priming CD8+ responses against pathogens not infecting DCs

7. Hypersensitivity Reactions

Type I (Immediate/Anaphylactic):

• IgE-mediated
• Allergen crosslinks IgE on mast cells/basophils
• Degranulation → histamine, leukotrienes
• Examples: Anaphylaxis, asthma, allergic rhinitis, food allergies
• Treatment: Epinephrine, antihistamines, corticosteroids

Type II (Cytotoxic/Antibody-mediated):

• IgG/IgM antibodies against cell surface antigens
• Mechanisms:
  • Complement activation → cell lysis
  • Opsonization → phagocytosis
  • ADCC
• Examples: Transfusion reactions, hemolytic disease of newborn, Goodpasture, Graves, Myasthenia gravis

Type III (Immune Complex):

• Antigen-antibody complexes deposit in tissues
• Complement activation
• Examples: Serum sickness, lupus, post-streptococcal glomerulonephritis, Arthus reaction
• Serums sickness: Fever, urticaria, arthralgia, proteinuria after 1-2 weeks

Type IV (Delayed-Type/Cell-mediated):

• T cell-mediated (no antibodies)
• Takes 24-72 hours to develop
• Examples: TB skin test (PPD), contact dermatitis (poison ivy), transplant rejection, granulomas

8. Major Histocompatibility Complex (MHC)

HLA (Human Leukocyte Antigen):

• Encoded by MHC on chromosome 6
• Most polymorphic genes in human genome

Class I (HLA-A, B, C):

• Heavy chain (α) + β2-microglobulin
• Presents to CD8+

Class II (HLA-DP, DQ, DR):

• α and β chains
• Presents to CD4+
• Linked to disease associations

HLA and Disease Associations:

• HLA-B27: Ankylosing spondylitis, reactive arthritis
• HLA-DR2: Multiple sclerosis, narcolepsy
• HLA-DR3: Type 1 diabetes, SLE
• HLA-DR4: Type 1 diabetes, rheumatoid arthritis
• HLA-DQ2/DQ8: Celiac disease

Transplant Matching:

• HLA matching important for solid organ transplants
• ABO matching essential
• Crossmatch to detect preformed antibodies

9. Tolerance and Autoimmunity

Central Tolerance:

• In thymus: Negative selection of self-reactive T cells
• In bone marrow: Negative selection of self-reactive B cells
• Deletes high-affinity self-reactive cells

Peripheral Tolerance:

• Anergy (functional inactivation without co-stimulation)
• Regulatory T cells (Tregs): FOXP3+, suppress responses
• Immune privilege (eyes, testes, brain)
• Clonal deletion (activation-induced cell death)

Autoimmunity:

• Loss of tolerance
• Genetic predisposition (HLA associations)
• Environmental triggers (infections, molecular mimicry)
• Examples: Hashimoto’s, Graves’, Myasthenia gravis, Guillain-Barré

10. Vaccines

Live Attenuated:

• Weakened pathogen
• Strong immune response, long-lasting immunity
• Cannot give to immunocompromised
• Examples: MMR, varicella, rotavirus, yellow fever, BCG

Inactivated/Killed:

• Pathogen killed (formalin)
• Safer, but weaker immune response
• Booster needed
• Examples: Hepatitis A, IPV (inactivated polio), rabies, influenza (injectable)

Subunit/Conjugate:

• Only antigenic components
• Example: Hepatitis B (HBsAg), HPV (L1 protein), Hib conjugate, pneumococcal conjugate

Toxoid:

• Inactivated toxin
• Example: Tetanus, diphtheria

mRNA Vaccines:

• Nucleic acid vaccine
• Encode antigen in lipid nanoparticles
• Pfizer/Moderna COVID-19 vaccines

Herd Immunity: When sufficient population is immune, transmission chain breaks, protecting vulnerable

Practice Questions for NEET PG

1. Compare and contrast innate and adaptive immunity.
2. Describe the process of T cell activation and differentiation.
3. Explain the four types of hypersensitivity reactions with examples.
4. Discuss the role of the complement system in immunity.
5. What are the mechanisms of vaccine-induced immunity?

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