The Gell and Coombs classification of hypersensitivity reactions places contact dermatitis to nickel in which type, and what is the characteristic effector cell?
- A Type I — mast cells degranulating after IgE cross-linking
- B Type IV — CD4+ Th1 cells sensitized to nickel-MHC-II complexes releasing IFN-γ ✓
- C Type II — cytotoxic T cells directly killing nickel-haptenized keratinocytes
- D Type III — immune complex deposition in the dermis
Explanation
Contact dermatitis (e.g., to nickel, poison ivy, chromate) is a classic Type IV (delayed-type, cell-mediated) hypersensitivity reaction. Nickel ions act as haptens binding to skin proteins; Langerhans cells present these modified peptides on MHC-II to CD4+ Th1 cells during sensitization. On re-exposure, memory Th1 cells release IFN-γ and TNF-α, activating macrophages and causing the eczematous skin reaction peaking at 48–72 hours. CD8+ cytotoxic T cells can also contribute in some contact reactions but CD4+ Th1 are primary.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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