Immunology for Microbiology
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Direct answer
Innate immunity answers within minutes — barriers, phagocytes, natural killer cells, complement and inflammation, without memory — while adaptive immunity brings T and B lymphocytes with clonal specificity and long-lived memory, days later but forever after. Complement can be activated by antibody (classical, via C1q binding IgG or IgM), by microbial surfaces directly (alternative), or by mannose-binding lectin, converging on C3 and the membrane attack complex; its fragments do the bedside work, C3b opsonising and C5a drawing neutrophils. MHC class I presents endogenous antigen to CD8 cells from every nucleated cell, MHC class II presents exogenous antigen to CD4 cells on professional antigen-presenting cells — the architecture behind viral killing, intracellular bacteria and the Gell–Coombs hypersensitivity ladder.
What you must remember
- Complement pathways: classical — immune complexes activate C1qrs; alternative — C3b deposits on microbial surfaces without antibody, amplified by factor B, factor D and properdin; lectin pathway — mannose-binding lectin with MASP enzymes.
- Convertases and effectors: classical/lectin C3 convertase is C4b2a, alternative is C3bBb; C3b is the opsonin, C5a the chemotaxin and anaphylatoxin (with C3a, C4a), and C5b–9 the membrane attack complex punching osmotic holes.
- Deficiency patterns: C3 deficiency — recurrent pyogenic infections; late-component C5–C9 deficiency — recurrent Neisseria meningitidaemia with otherwise normal health; properdin deficiency is X-linked; C1-inhibitor deficiency gives hereditary angio-oedema.
- MHC restriction: class I on all nucleated cells plus platelets, loaded with endogenous (viral, tumour) peptide, surveyed by CD8; class II on dendritic cells, macrophages and B cells, loaded with engulfed exogenous peptide, surveyed by CD4.
- Lymphocyte education: T cells mature in the thymus (positive selection for self-MHC, negative selection against self-reactivity); B cells in the marrow; NK cells kill MHC-I-negative stressed cells.
- Gell–Coombs ladder: type I — IgE on mast cells, immediate weal and flare, anaphylaxis and asthma; type II — IgG/IgM against cell-bound antigen, haemolytic disease of the newborn and autoimmune haemolysis; type III — immune-complex deposition, post-streptococcal glomerulonephritis, serum sickness, Arthus reaction; type IV — delayed, T-cell mediated, read at 48–72 hours: the tuberculin (Mantoux) test, contact dermatitis and graft rejection.
- Primary immunodeficiency signatures: Bruton's X-linked agammaglobulinaemia — boys over six months with recurrent pyogenic infections after maternal IgG wanes, absent tonsils and B cells; DiGeorge syndrome (22q11) — thymic aplasia with neonatal tetany and viral/fungal susceptibility; SCID — severe combined defects, in India flagged by disseminated BCG (BCGitis) after neonatal vaccination; hyper-IgM with opportunistic Pneumocystis; chronic granulomatous disease — catalase-positive staphylococci and Aspergillus, abnormal nitroblue tetrazolium test.
Mapping an infection pattern to a defect
Work backwards from the organism. Recurrent pus-forming sinopulmonary infection in a toddler whose tonsils are absent points to antibody failure — Bruton's; quantify immunoglobulins and look for B cells. Recurrent meningococcaemia in a well-grown teenager points to terminal complement; order CH50, which will be near zero. Chronic catalase-positive abscesses with lymphadenitis in a boy whose NBT test fails to reduce the dye is chronic granulomatous disease. An Indian infant with persistent BCG site discharge and disseminated lesions raises SCID until excluded — a programme-relevant clue, since BCG is given at birth in India. Each organism list is a shortcut to the defective arm: extracellular pyogens to antibody and complement, intracellular and fungal to T cells and macrophages.
Where students slip
The Mantoux test is labelled type III immune-complex — it is type IV delayed hypersensitivity, read as induration at 48–72 hours, which is also why it cannot be "read tomorrow". Anaphylatoxins (C3a, C4a, C5a) get mixed with opsonins; only fragments with chemotactic and mast-cell-degranulating activity are anaphylatoxins. And remember class I versus class II by target: endogenous-to-CD8, exogenous-to-CD4 — options shuffle these pairings in nearly every paper.
Frequently asked questions
Which complement fragment is the major opsonin?
C3b, which coats microbial surfaces and engages complement receptors on phagocytes; C5a meanwhile drives chemotaxis and mast-cell degranulation.
What infection pattern suggests terminal complement deficiency?
Recurrent invasive Neisseria infections — meningococcaemia and meningitis — in an otherwise healthy person; CH50 screening is near absent.
Why is the Mantoux test classified as type IV hypersensitivity?
It is T-cell-mediated delayed hypersensitivity to tuberculin protein, maximally indurated 48–72 hours after intradermal injection, with no antibody involvement.
How do MHC class I and II differ in antigen source?
Class I presents endogenously synthesised peptide (viruses, tumours) to CD8 cells on all nucleated cells; class II presents engulfed exogenous antigen to CD4 cells on professional antigen-presenting cells.
What marks Bruton's agammaglobulinaemia clinically?
Recurrent pyogenic infections beginning after six months of age in a boy, with absent tonsils and lymphoid tissue, profoundly low immunoglobulins and absent B cells.