• Mechanism
    • Antibody-mediated (IgG/IgM) binding to fixed antigens on cells/tissues.
    • Mnemonic: “Cy-2-toxic”.
    • Three main pathological processes:
      1. Phagocytosis & Opsonization/Complement Activation: Ab binds cell → complement activation (C3b) → MAC complex lysis or phagocytosis (e.g., AIHA).
      2. Antibody-Dependent Cellular Cytotoxicity (ADCC): NK cells bind Fc region of IgG → release granules (perforin/granzymes) → apoptosis.
      3. Cellular Dysfunction (Non-cytotoxic): Ab binds receptors, either blocking or stimulating function without destroying the cell (e.g., Myasthenia Gravis, Graves).
  • High-Yield Examples
    • Hematologic:
      • Autoimmune Hemolytic Anemia: (+) Direct Coombs.
      • ITP: Anti-platelet antibodies.
      • Acute Transfusion Reactions & Hemolytic Disease of Newborn.
    • Tissue Specific:
      • Goodpasture Syndrome: Anti-GBM (Type IV collagen). Linear IF. Hemoptysis + Hematuria.
      • Rheumatic Fever: Molecular mimicry (Strep M protein).
    • Blistering Skin Disorders:
      • Pemphigus Vulgaris: Anti-desmoglein. (+) Nikolsky.
      • Bullous Pemphigoid: Anti-hemidesmosome. (-) Nikolsky.
    • Receptor Dysfunction (Non-cytotoxic):
      • Graves Disease: Stimulating TSH receptor Abs.
      • Myasthenia Gravis: Blocking ACh receptor Abs.
  • Key Distinction
    • Type II = Antibodies against FIXED antigens (e.g., on a cell).
    • Type III = Antibodies against SOLUBLE antigens (immune complexes deposit later).