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Discussion

ACD is elicited in sensitized individuals upon allergen re-exposure, leading to innate and adaptive immune activation. The inflammatory milieu during the elicitation phase is historically thought to be Th1 predominant, although recent work also implicates Th17 and Th22 cytokines. 1 These reactions are likely hapten specific 1; for instance, contact allergy to nickel correlates with a mixed Th1/Th2 response. 1, 2 After prolonged and repeated allergen exposure, a Th2-predominant response is observed in chronic lesions of ACD. 3