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-YieldNEET PG
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.
