## Type I Hypersensitivity: Immunoglobulin Role ### Correct Statements (Options 0, 1, 2) **Key Point:** Type I hypersensitivity is fundamentally an **IgE-mediated** reaction, not IgG-mediated. | Feature | Details | |---------|----------| | **Primary Ig** | IgE (binds to FcεRI on mast cells/basophils) | | **Effector Cells** | Mast cells (tissue), basophils (blood) | | **Receptor** | High-affinity FcεRI (cross-linking triggers degranulation) | | **Mediator Release** | Within seconds to minutes (histamine, tryptase, leukotrienes) | **High-Yield:** The hallmark of Type I is **IgE-mediated, immediate-onset** response. Sensitization occurs on first exposure; clinical reaction on re-exposure. ### Why Option 3 Is Incorrect **IgG is NOT the predominant immunoglobulin in Type I hypersensitivity.** IgG plays a role in: - Type II cytotoxic hypersensitivity (antibody-mediated cell destruction) - Type III immune complex disease (IgG + antigen → circulating immune complexes) - Type IV delayed-type hypersensitivity (IgG does NOT participate; this is T-cell mediated) **Clinical Pearl:** While IgG antibodies can form against allergens (e.g., in chronic allergen exposure), they do NOT trigger the acute degranulation characteristic of Type I reactions. IgE is the sole mediator of immediate hypersensitivity. ### Mnemonic: **IgE = Immediate** IgE → Immediate hypersensitivity (Type I). Think: **E**mergency response. [cite:Robbins 10e Ch 6]
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