## Cytokine Profile in Type IV Hypersensitivity **Key Point:** Type IV hypersensitivity (delayed-type, cell-mediated) is driven by Th1 and cytotoxic T lymphocytes (CTLs) that produce IFN-γ and TNF-α, which activate macrophages and induce local inflammation. ### Mechanism Type IV hypersensitivity involves: 1. Antigen presentation to T cells via MHC class I and II molecules 2. Activation of Th1 cells and CTLs 3. Release of **IFN-γ** (activates macrophages, increases MHC expression) 4. Release of **TNF-α** (promotes inflammation, endothelial activation) 5. Recruitment and activation of macrophages → tissue damage **High-Yield:** IFN-γ is the hallmark cytokine of Type IV hypersensitivity and is used diagnostically in tuberculin skin tests and interferon-gamma release assays (IGRAs). ### Comparison with Other Hypersensitivity Types | Type | Mechanism | Key Mediators | |------|-----------|---------------| | Type I (Immediate) | IgE-mediated mast cell degranulation | Histamine, tryptase, leukotrienes | | Type II (Cytotoxic) | IgG/IgM antibody-mediated | Complement, ADCC, antibodies | | Type III (Immune Complex) | Circulating immune complex deposition | Complement (C3a, C5a), IgG | | Type IV (Delayed) | T cell-mediated | **IFN-γ, TNF-α** | **Clinical Pearl:** Type IV reactions typically peak 48–72 hours after antigen exposure, unlike Type I which occurs within minutes. This delayed kinetics reflects the time needed for T cell recruitment and macrophage activation.
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