- Mechanism
- Antibody-mediated (IgG/IgM) binding to fixed antigens on cells/tissues.
- Mnemonic: “Cy-2-toxic”.
- Three main pathological processes:
- Phagocytosis & Opsonization/Complement Activation: Ab binds cell → complement activation (C3b) → MAC complex lysis or phagocytosis (e.g., AIHA).
- Antibody-Dependent Cellular Cytotoxicity (ADCC): NK cells bind Fc region of IgG → release granules (perforin/granzymes) → apoptosis.
- 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).