Immunology
Architecture of the immune response
Innate immunity (barriers, complement, phagocytes, NK cells) acts within minutes without memory. Adaptive immunity is clonal, specific, and remembers: B cells make antibody and CD4+ T cells orchestrate while CD8+ T cells kill. Know the immunoglobulin classes - IgM (primary response, pentamer, best complement activator), IgG (placental transfer, opsonization), IgA (mucosal, dimeric with J chain), IgE (mast cell sensitization), IgD (B cell receptor).
Hypersensitivity, the classic four
Type I immediate IgE (anaphylaxis, allergic rhinitis); Type II antibody against cell-bound antigen (autoimmune hemolytic anemia, Goodpasture, hemolytic transfusion reaction); Type III immune complex (serum sickness, SLE nephritis, Arthus); Type IV delayed, T-cell mediated (PPD, contact dermatitis, transplant rejection).
Immunoassays and their failure modes
Sandwich ELISA reads high when antigen is high; competitive ELISA reads low when analyte is high. Extremely high antigen can saturate both antibodies and produce a falsely low sandwich result (hook effect). Excess antibody in agglutination tests can block lattice formation (prozone), seen classically in syphilis serology and Brucella. Nephelometry measures light scatter, flow cytometry measures single cells, and immunofluorescence uses fluorochrome-labeled antibody.
Traps
ANA is sensitive but not specific; anti-dsDNA and anti-Smith are specific for SLE. Rheumatoid factor can cause false positives in many immunoassays. Do not confuse primary immunodeficiency (Bruton agammaglobulinemia, SCID, DiGeorge, chronic granulomatous disease) with secondary causes like HIV or malnutrition.
Worked example: a patient with penicillin-induced hemolytic anemia shows IgG and C3 on the DAT - a Type II reaction, not Type I or III.