## Type I Hypersensitivity: Mechanism and Characteristics ### Correct Statements (Options 0, 1, 3) **Key Point:** Type I hypersensitivity is an **IgE-mediated, immediate reaction** occurring within minutes of allergen exposure. | Feature | Details | | --- | --- | | **Mediator** | IgE antibodies (not IgG or IgM) | | **Effector cells** | Mast cells (tissue-resident) and basophils (circulating) | | **Timing** | Immediate: minutes (preformed mediators) to hours (newly synthesized) | | **Preformed mediators** | Histamine, tryptase, heparin, chymase | | **Newly synthesized mediators** | Leukotrienes (LTC₄, LTD₄, LTE₄), prostaglandins, PAF | **Clinical Pearl:** Histamine causes the classic triad: - Vasodilation → flushing, hypotension - Increased vascular permeability → angioedema, urticaria - Smooth muscle contraction → bronchospasm, laryngeal edema ### The Incorrect Statement (Option 2) **Warning:** Type I hypersensitivity is **NOT T cell-dependent**. It does NOT require antigen presentation on MHC Class II molecules. **High-Yield:** Type I is **antibody-mediated** (IgE) and **innate** in nature. T cells play a role in the **sensitization phase** (Th2 cells produce IL-4 and IL-5 to promote IgE class switching), but the acute reaction itself is **not T cell-dependent**. ### Distinction from Type IV Hypersensitivity | Feature | Type I | Type IV | | --- | --- | --- | | **Antibody** | IgE | None (cell-mediated) | | **Effector cells** | Mast cells, basophils | T cells (CD8^+^, CD4^+^) | | **MHC requirement** | No | Yes (MHC Class I & II) | | **Timing** | Minutes–hours | 24–72 hours | | **Example** | Anaphylaxis, urticaria | Contact dermatitis, TB skin test | **Mnemonic:** **IAMB** for Type I = **I**gE, **A**ntibody, **M**ast cells, **B**asophils (no T cells needed for the acute phase).
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