Reframing Eczema: Th2-Skewed Contact Sensitization, Atopy Patch Testing, and Systemic Contact Dermatitis.

purpose of reviewWe review allergic contact dermatitis (ACD) with predominant Th2 type cytokine expression in the context of chronic cutaneous inflammation. While more has been written about Th1 skewed ACD due to potent allergens in the setting of healthy skin, this review highlights recognition of Th2 skewed ACD in both atopic dermatitis and systemic contact dermatitis and the role of allergen avoidance as an alternative to systemic therapies. RECENT

findingsTh2 skewed ACD rarely occurs to potent allergens. It more commonly occurs in response to allergens considered “non-sensitizers” in the local lymph node assay. These sensitizers include weaker allergens (e.g. propylene glycol), larger molecules (e.g. food proteins) and commensal micro-organisms. Importantly, group 2 innate lymphoid cells and natural killer T cells may contribute to these cutaneous memory responses without education of Th2 cells in the local lymph node and without downstream antigen-specific IgE. The resulting intrinsic atopic dermatitis may be food-triggered and better diagnosed with atopy patch testing than with tests for antigen specific-IgE used for immediate type hypersensitivity reactions. Chronic contact, atopic, and stasis dermatitis all occur in the setting of irritant dermatitis and microbial dysbiosis. Both Th1 and Th2 cytokines mediate ACD, although those cytokines may arise from innate immune pathways and not exclusively from T helper cells educated in the local lymph node. More refinement and use of atopy patch tests to identify less potent allergens and dietary avoidance of patient-specific allergens may reduce the number of patients who require systemic therapy for eczema.