A Defective Inflammatory Response May Underlie Cases of Atopic Dermatitis

Abstract

An investigation of atopic dermatitis (AD) proposes an association between susceptibility to developing allergic contact sensitization (ACS) and a possible defect in the delayed hypersensitivity inflammatory response.¹ Current research supports the predominant pathogenesis of AD to be T-helper cell 2 (Th2)-mediated Type I hypersensitivity response and allergic contact dermatitis (ACD) to be a T-helper cell 1 (Th1)-mediated Type IV hypersensitivity response.²

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