Doctor’s Passport

Find your next topic

Explore the current textbook

Available drafts · Clinical review pending
Membership
Educational draft · awaiting clinical reviewUse Rapid for revision, not patient-care decisions. Check current national and local guidance and the BNF or BNFC before acting.
RapidMLAMRCPMRCS

Immunology

Essential points for quick revision.

Saved on this device

Synopsis

Connect immune recognition, signalling and effector pathways to infection control, hypersensitivity, autoimmunity, immunodeficiency, vaccination and the interpretation of common immune investigations.

  • Innate immunity responds rapidly through barriers, pattern-recognition receptors, phagocytes, natural killer cells, cytokines and complement; it also initiates adaptive responses.
  • Adaptive immunity uses clonally distributed antigen receptors: B cells generate antibody responses and T cells coordinate or kill through peptide–MHC recognition.
  • Antigen presentation on MHC I primarily engages CD8 T cells, while MHC II on professional antigen-presenting cells primarily engages CD4 T cells.

Reasoning priorities

01
Full blood count with differential

Quantify major circulating leukocyte populations and identify cytopenia or eosinophilia.

Use age-specific ranges and trends; normal counts do not prove normal cell function, and infection or medicines can cause secondary changes.

Worked reasoning

Worked exampleLocalise an immune-pathway defect

Inputs: a young adult has two episodes of invasive meningococcal disease, normal neutrophil count, normal quantitative immunoglobulins and no history of opportunistic infection.

  1. Map the organism and phenotype: repeated invasive Neisseria infection is a focused clue to impaired terminal complement-mediated killing rather than a general infection frequency label.
  2. Use existing normal data to reduce, not eliminate, major quantitative phagocyte and antibody deficits; absence of opportunistic infection makes profound T-cell failure less likely.
  3. Select pathway-level assessment with complement components and a validated functional assay, alongside evaluation for acquired complement consumption and the clinical infection pathway.
  4. Conclude that terminal complement deficiency is the leading mechanism requiring specialist confirmation, while immediate infection prevention and acute-care advice proceed through appropriate services.
  5. Verify by predicting the test pattern before results: impaired terminal pathway function with preserved upstream activation would fit; a global reduction should reopen consumption, liver production or sample issues.
Open full textbook Answer 2 questions
Sources and review status5 sources · checked 7 Sept 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 7 Sept 2026; clinical approval remains outstanding.

Authoring stateRapid draftClinical stateAwaiting reviewJurisdictionUnited Kingdom