## Type IV Hypersensitivity Cytokine Profile **Key Point:** IFN-γ is the hallmark cytokine of Type IV (delayed-type) hypersensitivity, secreted by activated Th1 cells and CD8+ T cells. ### Mechanism of IFN-γ in DTH 1. **Th1 activation** → IFN-γ production 2. **Macrophage activation** → enhanced antigen presentation and pro-inflammatory mediator release 3. **Local inflammation** → induration, erythema, and tissue damage (peaks at 48–72 hours) ### Cytokine Roles in Hypersensitivity | Cytokine | Hypersensitivity Type | Cell Source | Function | |----------|----------------------|-------------|----------| | **IFN-γ** | **Type IV (DTH)** | **Th1, CD8+ T cells** | **Macrophage activation, granuloma formation** | | IL-4 | Type II (Th2-driven) | Th2 cells | B cell activation, IgE production | | IL-5 | Type I (allergic) | Th2 cells | Eosinophil recruitment and activation | | TNF-α | Types I, II, III, IV | Multiple | Amplifies inflammation (not primary in DTH) | **High-Yield:** IFN-γ is the **defining cytokine** of Type IV hypersensitivity. Its presence distinguishes DTH from Type I (IgE-mediated) and Type II (antibody-mediated) reactions. **Clinical Pearl:** Tuberculin skin test (Mantoux test) is a classic example of Type IV hypersensitivity driven by IFN-γ-producing Th1 cells responding to *Mycobacterium tuberculosis* antigens. **Mnemonic:** **DTH = Th1 = IFN-γ** — Delayed-Type Hypersensitivity is a Th1-driven response powered by Interferon-gamma. [cite:Robbins 10e Ch 6]
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