Clinical Immunology and Immunopathology
Core concepts
Master the architecture of the immune response: innate versus adaptive, antigen presentation via MHC I and II, T-helper subsets, and immunoglobulin classes and functions. Understand complement pathways (classical, alternative, lectin) and the consequences of deficiency (C2/C4 for immune complex disease, C3 for recurrent pyogenic infection, terminal components for Neisseria). Know the primary immunodeficiency patterns: Bruton agammaglobulinaemia (absent B cells, low all immunoglobulins), DiGeorge syndrome (T-cell deficiency, hypocalcaemia), chronic granulomatous disease (defective oxidative burst), and complement deficiencies.
Hypersensitivity classification recurs: type I IgE-mediated, type II antibody-mediated, type III immune complex, type IV T-cell mediated. Autoimmune serology requires pattern recognition: ANA patterns, anti-dsDNA and anti-Sm in SLE, anti-centromere in limited scleroderma, anti-topoisomerase in diffuse disease, anti-Jo-1 in myositis, and ANCA patterns (c-ANCA/PR3 versus p-ANCA/MPO).
Traps in questions
A positive ANA is common in healthy people; it supports but does not confirm lupus. ANCA positivity without clinical correlation is nonspecific. Do not confuse type II (fixed tissue antigen) with type III (circulating immune complexes). In transplantation, hyperacute rejection is antibody-mediated and preformed; acute cellular rejection is T-cell mediated.
Rule of thumb
When a question describes a reaction within minutes of exposure, think type I; hours to days with immune complexes, think type III; days with T cells (contact dermatitis, graft rejection), think type IV.