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BiologyHuman Health and Disease
Which of the following are components of innate immunity?
A. Antibody production by B cells
B. T-cell mediated cytotoxicity
C. Natural killer cells
D. Complement proteins
Options
1
A and B only
2
A, B and C only
3
C and D only
4
All of the above
Correct Answer
C and D only
Solution
1

Innate = non-specific, no memory, immediate response.

A: Antibody production by B cells = adaptive immunity ✗

B: T-cell cytotoxicity = adaptive immunity ✗

2

C: Natural killer cells = innate immunity ✓

D: Complement proteins = innate immunity ✓

Answer: C and D only

Innate: NK cells, complement, macrophages, neutrophils, interferons
Adaptive: B cells (antibodies), T cells (cytotoxicity)
Theory: Human Health and Disease
1. Overview of Immune System

Two major arms: Innate immunity (non-specific, immediate): physical barriers, cellular components (phagocytes, NK cells), humoral components (complement, interferons, antimicrobial peptides). No memory. Adaptive immunity (specific, slower, with memory): lymphocytes (T cells, B cells). Antigen-specific. Memory = faster/stronger response on re-exposure. Primary response: first exposure to antigen. Slow (5-10 days to peak). Mostly IgM. Secondary (anamnestic) response: re-exposure. Fast (1-3 days). Higher titer. Mostly IgG. Immunological memory (long-lived B and T memory cells).

2. Components of Innate Immunity

Physical barriers: skin (keratin layer), mucous membranes (respiratory, GI tracts), cilia (sweep pathogens out of airways), acid (stomach pH 1.5-2, vaginal pH 3.8-4.5), lysozyme (tears, saliva - cleaves bacterial cell walls), antimicrobial peptides (defensins, cathelicidins). Cellular components: Neutrophils: most abundant WBC (60-70%). First responders. Phagocytose and kill bacteria (oxidative burst, lysosomal enzymes). Short-lived (5-10 hours). Macrophages: in tissues. Phagocytose, present antigens (MHC II). Produce cytokines (TNF-alpha, IL-1, IL-6, IL-12). Natural Killer (NK) cells: kill virus-infected cells and tumour cells without prior sensitisation. Dendritic cells: bridge innate and adaptive. Sample antigens, migrate to lymph nodes, present to T cells. Eosinophils: against parasites. Mast cells/Basophils: allergic responses.

3. Complement System

Complement: ~30 serum proteins (C1-C9, factors B, D, P, H, I, etc.). Three activation pathways: Classical: C1q binds antibody-antigen complex. Requires adaptive immunity. Lectin: MBL (mannose-binding lectin) binds mannose on microbial surfaces. Alternative: C3 spontaneous hydrolysis + pathogen surfaces amplify. All converge at C3 convertase → C3 → C3a + C3b. C3b: opsonin (coats bacteria, enhances phagocytosis). C3a, C5a: anaphylatoxins (trigger mast cell degranulation, chemotaxis of neutrophils). Membrane attack complex (MAC): C5b-6-7-8-9 forms pore in bacterial membrane → lysis. Complement deficiencies: C1q deficiency → increased susceptibility to SLE (systemic lupus). C3 deficiency → severe recurrent infections. C5-9 deficiencies → Neisseria (meningitis, gonorrhoea) susceptibility.

4. Adaptive Immunity

Specific, memory-based response. Antigens trigger clonal selection: antigen-specific lymphocytes multiply. Humoral immunity (B cells): B cells + antigen + helper T cell signals → plasma cells (antibody factories). IgM first produced (pentamer, 10 binding sites). Class switching (with T cell help): IgG, IgA, IgE. Memory B cells persist. Cell-mediated immunity (T cells): CD4+ helper T (Th) cells: activate macrophages (Th1, for intracellular pathogens), help B cells (Th2). CD8+ cytotoxic T (CTL) cells: kill virus-infected cells and tumour cells. Direct contact. Perforin/granzymes. Regulatory T cells (Tregs): suppress immune responses, prevent autoimmunity. T cell activation requires: antigen presented on MHC + co-stimulatory signals (CD28-B7).

5. Antibodies (Immunoglobulins)

Structure: Y-shaped. 2 heavy chains + 2 light chains (H2L2). Constant region (Fc): determines antibody class. Fab region: antigen-binding. Variable region (VH + VL): determines antigen specificity. 5 classes: IgG: most abundant (75%). 4 subclasses. Crosses placenta (passive immunity to newborn). Opsonin. Activates complement. IgA: secretory (in tears, saliva, breast milk, mucus). Protects mucosal surfaces. IgM: first produced in primary response. Pentamer. Best complement activator. IgE: allergy and parasites. Binds mast cells/basophils. IgD: B cell surface receptor. Antibody functions: neutralisation (block pathogen attachment), opsonisation (enhance phagocytosis), complement activation, ADCC (antibody-dependent cell cytotoxicity). Monoclonal antibodies: therapeutic (Rituximab for lymphoma - anti-CD20, Trastuzumab/Herceptin for breast cancer - anti-HER2, Adalimumab for RA/Crohn's - anti-TNF).

6. Vaccines and Active Immunity

Vaccination: deliberate introduction of antigen to stimulate adaptive immune response without disease. Types: Live attenuated: weakened pathogen. BCG (TB), MMR (measles/mumps/rubella), oral polio (Sabin), varicella. Strong immunity, sometimes revert to virulence. Killed/inactivated: whole pathogen killed. Salk polio (IPV), hepatitis A, rabies, influenza. Safer but weaker. Subunit: specific antigens only. HBsAg (hepatitis B), Pneumovax (polysaccharide), HPV (Gardasil - VLPs). Toxoid: inactivated toxin. Diphtheria and tetanus vaccines. mRNA vaccines (COVID-19: Pfizer-BioNTech, Moderna): mRNA for spike protein → cells produce antigen → immune response. No live pathogen, no DNA. Nobel Prize 2023: Katalin Kariko and Drew Weissman for mRNA vaccine technology. India vaccines: BCG, DTP, OPV, HBV, Hib, IPV, Rotavirus, PCV, MR, JE, typhoid.

7. Disorders of the Immune System

Hypersensitivity (allergy): exaggerated immune response to harmless antigens (allergens). Type I (immediate): IgE-mediated. Mast cell degranulation → histamine, leukotrienes → vasodilation, smooth muscle contraction. Hay fever, asthma, food allergies, anaphylaxis. Treatment: antihistamines, corticosteroids, adrenaline (anaphylaxis). Type II (cytotoxic): antibody (IgG/IgM) against cell surface antigens. Haemolytic disease of newborn, ABO incompatibility transfusion reaction, myasthenia gravis. Type III (immune complex): antigen-antibody complexes deposit in tissues. Serum sickness, SLE, post-streptococcal glomerulonephritis. Type IV (delayed): T-cell mediated. Contact dermatitis (poison ivy, nickel allergy), PPD test for TB, type 1 diabetes (insulin-producing cells destroyed by CTL). Autoimmune diseases: immune system attacks self-antigens. SLE (anti-DNA antibodies), rheumatoid arthritis (anti-CCP), Type 1 diabetes (anti-islet cells), MS (anti-myelin), Hashimoto thyroiditis.

8. HIV/AIDS

HIV (Human Immunodeficiency Virus): lentivirus (retrovirus). Two types: HIV-1 (pandemic) and HIV-2 (West Africa, less virulent). Genome: 2 copies of ssRNA (~9.7 kb) encoding gag, pol, env genes. Transmission: sexual contact, blood (transfusions, needles), vertical (mother to child during birth or breastfeeding). Target: CD4+ T cells, macrophages, dendritic cells. Entry: gp120 (envelope protein) binds CD4 + CCR5 or CXCR4 co-receptor. gp41 mediates fusion. Replication: reverse transcriptase (RNA→DNA), integrase (integrates into host chromosome = provirus), protease (cleaves polyproteins). HIV disease progression: Acute infection (flu-like, high viraemia, CD4 fall). Chronic asymptomatic phase (years). AIDS (CD4 < 200 cells/microL + AIDS-defining illness). Opportunistic infections: Pneumocystis jirovecii pneumonia, CMV retinitis, toxoplasmosis, Cryptococcus meningitis, MAC, Kaposi sarcoma (HHV-8), oral candidiasis. Treatment: ART (antiretroviral therapy) - NRTI + NNRTI + PI or INSTI combinations. Undetectable = untransmittable (U=U).

Frequently Asked Questions
1. What is the difference between innate and adaptive immunity? ⌄
Innate immunity: present from birth (not acquired). Non-specific (responds to broad molecular patterns = PAMPs on pathogens, recognised by PRRs - pattern recognition receptors like Toll-like receptors). Responds within minutes to hours. No memory. Components: barriers (skin), phagocytes (neutrophils, macrophages), NK cells, complement, interferons. Adaptive immunity: develops after exposure. Highly specific (responds to specific antigens). Slower (days to weeks for primary response). Has memory (faster, stronger on re-exposure). Components: B cells (antibodies = humoral), T cells (cell-mediated = CD4+ helpers, CD8+ killers, Tregs). Interaction: innate immunity initiates and shapes adaptive response. Dendritic cells sample pathogens, process antigens, present on MHC to naive T cells in lymph nodes (antigen presentation). Cytokines from innate cells (IL-12, IL-4, etc.) direct T helper cell differentiation.
2. How do natural killer cells distinguish healthy cells from infected/tumour cells? ⌄
NK cells use a "missing self" model. Healthy cells: express MHC class I (HLA-A, B, C) on surface. MHC-I on healthy cell binds inhibitory receptors on NK cell (KIR = killer-cell immunoglobulin-like receptor) → NK cell inhibited, does not kill. Virus-infected cells: many viruses downregulate MHC-I to hide from CD8+ T cells. Result: less MHC-I on infected cell → fewer inhibitory signals to NK cell → NK cell activating receptors dominate → NK cell kills infected cell. Tumour cells: often lose MHC-I expression during malignant transformation → NK cell kills. Activation receptors on NK cells (NKG2D, NCRs): recognise stress ligands (MICA/MICB, ULBP) upregulated on infected/transformed cells. Mechanism of killing: NK cell forms immunological synapse with target. Releases perforins (form pores in target membrane) and granzymes (serine proteases that enter through perforin pores, activate caspases → apoptosis).
3. What are interferons and how do they protect against viral infections? ⌄
Interferons (IFNs): cytokines produced by cells in response to viral infection. Named because they "interfere" with viral replication. Three types: Type I IFNs (IFN-alpha and IFN-beta): produced by virus-infected cells (innate response). Bind IFN receptors on adjacent cells → JAK-STAT signalling → antiviral state. Antiviral state: upregulates: PKR (protein kinase R - inhibits translation), RNase L (degrades viral RNA), Mx proteins (block viral replication), upregulates MHC-I (enhances CTL recognition). Type II IFN (IFN-gamma): produced by T cells and NK cells. Activates macrophages (key for intracellular pathogens like Mycobacterium, Listeria). Type III IFNs (IFN-lambda): mainly at epithelial surfaces, less inflammatory. Clinical use: IFN-alpha: treatment of chronic hepatitis B and C (before direct-acting antivirals), hairy cell leukaemia, melanoma. IFN-beta: multiple sclerosis (reduces relapse rate). The COVID-19 pandemic highlighted: SARS-CoV-2 actively suppresses type I IFN signalling → severe cases characterised by delayed IFN response + excessive inflammatory cytokines (cytokine storm).
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