Unbalanced aryl hydrocarbon receptor expression in peripheral and lesional T cell subsets of atopic dermatitis

Conclusion: AhR was highly expressed in subpopulations of T cells in peripheral blood and skin lesions of AD, suggesting that AhR might contribute to the pathogenesis of AD. Background: and Objective The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor, which is involved in the pathogenesis of a variety of skin diseases such as atopic dermatitis (AD). In this study, we aimed to study the AhR-expressing cells in T helper 17 (Th17), T helper 22 (Th22), regulatory T cells (Treg) and B cells in peripheral blood and in AD skin lesions. Methods: Twenty AD patients defined according to the Chinese criteria of atopic dermatitis and eighteen healthy subjects were included in our study. The AhR-expressing Th17, Th22, Treg and total B cells in peripheral blood was measured by flow cytometry. The AhR + Th17 cells and AhR + Th22 cells in AD skin lesions was measured by immunofluorescence. The mRNA of AhR, interleukin (IL)-22, IL-17A, IL-10, Foxp3, RORγT and TGF-β in peripheral blood mononuclear cells (PBMCs) was measured by real-time quantitative polymerase chain reaction. Results: The expression of AhR in peripheral CD4 + T cells, Th22 cells, Treg cells and total B cells was significantly increased in AD. AhR + IL-17A + and AhR + IL-22 + lymphocytes were also increased in AD skin lesions. The mRNA levels of AhR, IL-22 and IL-17A in PBMCs in AD patients were significantly higher. AhR mRNA levels in PBMCs positively correlated with peripheral basophil count, peripheral eosinophils count and mRNA levels of IL-22.