In Type II hypersensitivity reactions, which of the following mechanisms is NOT involved in antibody-mediated cellular injury?

Explanation

## Mechanisms of Type II Hypersensitivity **Key Point:** Type II hypersensitivity is antibody-mediated (IgG or IgM) against cell surface or tissue-bound antigens. Mast cell degranulation is characteristic of Type I (immediate) hypersensitivity, NOT Type II. ### Three Main Mechanisms in Type II Hypersensitivity 1. **Complement-Dependent Cytotoxicity (CDC)** - IgG or IgM binds to cell surface antigen - Activates classical complement cascade (C1q binding) - Forms membrane attack complex (MAC) - Results in cell lysis - Example: Hemolytic transfusion reactions, autoimmune hemolytic anemia 2. **Antibody-Dependent Cellular Cytotoxicity (ADCC)** - IgG-coated target cell binds Fc receptors on NK cells, macrophages, or neutrophils - Triggers cytotoxic granule release - Example: Graves' disease (TSH receptor antibodies), Goodpasture syndrome 3. **Opsonization and Phagocytosis** - IgG-coated cells are recognized by Fc receptors on macrophages and neutrophils - Cells are engulfed and destroyed - Example: Autoimmune hemolytic anemia, immune thrombocytopenia ### Why Mast Cell Degranulation is NOT Type II **High-Yield:** Mast cell degranulation is the **hallmark of Type I hypersensitivity**, triggered by cross-linking of IgE on mast cell surfaces. This releases histamine, tryptase, leukotrienes, and prostaglandins — causing immediate symptoms (minutes to hours). Type II reactions are slower (hours to days) and do not involve mast cells. ### Comparison Table: Type I vs Type II | Feature | Type I | Type II | |---------|--------|--------| | **Antibody** | IgE | IgG, IgM | | **Cells Involved** | Mast cells, basophils | Macrophages, NK cells, complement | | **Mechanism** | Mast cell degranulation | CDC, ADCC, opsonization | | **Onset** | Minutes | Hours to days | | **Example** | Anaphylaxis, urticaria | Hemolytic anemia, Graves' disease | **Mnemonic:** **Type II = Antibody-to-Cell** (IgG/IgM against cell surface) → CDC, ADCC, opsonization. **Type I = IgE** → mast cell degranulation. **Clinical Pearl:** In Graves' disease, TSH receptor antibodies (IgG) bind to thyroid follicular cells and activate them via ADCC and opsonization, NOT mast cell degranulation. [cite:Robbins 10e Ch 6]