Distinct Superficial Epidermal Expression Patterns of IL-19 and IL-37 in Atopic Dermatitis

Atopic dermatitis (AD) is characterized by heterogeneous immune activation extending beyond clinically apparent lesions. Interleukin-19 (IL-19) has been implicated in cytokine-responsive keratinocyte activation, whereas interleukin-37 (IL-37) has endogenous anti-inflammatory functions. Their superficial epidermal expression patterns in lesional and clinically non-lesional AD skin have not been extensively characterized within the same cohort. To compare IL19 and IL37 mRNA expression in lesional and clinically non-lesional, lesion-adjacent AD skin with healthy control skin and to explore associations between transcript abundance and clinical characteristics. In this exploratory cross-sectional study, tape strip samples were collected from lesional and clinically non-lesional skin of 32 patients with AD and from corresponding skin of 35 healthy controls. IL19 expression did not differ significantly among healthy control, lesional, and clinically non-lesional AD skin in the overall cohort. In contrast, IL37 transcript abundance was significantly higher in lesional AD skin than in healthy control skin (p = 0.0002) and was also increased in clinically non-lesional skin (p = 0.0387). In severity-stratified analyses, lesional IL37 expression was increased in both moderate and severe-to-very severe AD, whereas lower lesional IL19 expression relative to healthy control skin was observed in severe-to-very severe AD (p = 0.0412). Lesional IL19 expression showed an inverse association with EASI severity category (p = 0.045), while lesional IL37 expression was positively associated with sleep-disturbance scores (p = 0.0203). The two transcripts showed distinct expression patterns in this cohort. Increased IL37 mRNA was compatible with, but did not establish, a compensatory response extending into lesion-adjacent clinically non-lesional skin. Overall IL19 upregulation was not detected, and lower lesional expression was observed in severe-to-very severe AD. However, these exploratory observations do not establish cytokine function or validate either transcript as a stand-alone biomarker.