# Immunology for Microbiology

> Immunology essentials for FMGE Microbiology: innate versus adaptive, complement pathways, MHC restriction, hypersensitivity types and immunodeficiency patterns.

- Canonical URL: https://prepelephant.com/topics/fmge/microbiology/immunology-micro-fmge
- Exam / course: FMGE · Subject: Microbiology
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Immunology for Microbiology", PrepElephant, https://prepelephant.com/topics/fmge/microbiology/immunology-micro-fmge

## 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.