## Type II Hypersensitivity: Mechanism Overview **Key Point:** Type II hypersensitivity is antibody-mediated cytotoxicity primarily driven by IgG and IgM antibodies, NOT IgE. IgE is the hallmark mediator of Type I (immediate) hypersensitivity. ### Correct Mechanisms in Type II Hypersensitivity | Mechanism | Antibody | Outcome | |-----------|----------|----------| | Complement activation | IgG, IgM | MAC formation → cell lysis | | ADCC | IgG (Fc binds NK cells, macrophages) | Antibody-dependent killing | | Opsonization | IgG | Enhanced phagocytosis by neutrophils, macrophages | | Receptor blockade | IgG | Functional impairment (e.g., myasthenia gravis) | **High-Yield:** Type II hypersensitivity antibodies are **IgG and IgM**, never IgE. IgE is exclusively Type I. ### Classic Examples of Type II Hypersensitivity - Graves' disease (stimulating antibodies to TSH receptor) - Goodpasture syndrome (anti-basement membrane IgG) - Autoimmune hemolytic anemia (IgG anti-RBC) - Pemphigus vulgaris (anti-desmoglein IgG) - Transfusion reactions (ABO incompatibility) **Clinical Pearl:** In Type II hypersensitivity, the target cell or tissue is destroyed by antibody binding followed by complement activation or cell-mediated cytotoxicity — NOT by mast cell degranulation or immediate release of histamine. **Warning:** Do NOT confuse Type I (IgE-mediated, mast cells, immediate) with Type II (IgG/IgM-mediated, antibody-dependent cytotoxicity, delayed minutes to hours).
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