Abstract: Most current studies suggest that alopecia areata is an autoimmune disease mediated by Th1 cells, and that atopic dermatitis is a classic Th2 cell-led inflammatory disease. Recent studies have also shown a potential role of the Th2 axis in the onset of alopecia areata, with significant elevation of Th2-associated biomarkers found in the scalp and serum. In addition, GWAS also identified susceptibility loci for Th2 (IL-4 and IL-13) in alopecia areata. Patients with concurrent FLG mutations are more likely to develop severe alopecia areata. The therapeutic efficacy of duplizumab and JAK inhibitors in alopecia areata with atopic dermatitis suggests the contribution of different cytokine pathways to the alopecia areata phenotype and contributing to the future selection of alopecia areata-targeted therapeutic.

Key words: alopecia areata, atopic dermatitis, correlation, complications, duplizumab