IL-38 Aggravates Atopic Dermatitis via Facilitating Migration of Langerhans cells.

ABSTRACT: Atopic dermatitis (AD) is a common inflammation skin disease that involves dysregulated interplay between immune cells and keratinocytes. Interleukin-38 (IL-38), a poorly characterized IL-1 family cytokine, its role and mechanism in the pathogenesis of AD is elusive. Here, we show that IL-38 is mainly secreted by epidermal keratinocytes and highly expressed in the skin and downregulated in AD lesions. We generated IL-38 keratinocyte-specific knockout mice (K14^Cre/+-IL-38^f/f ) and induced AD models by 2,4-dinitrofluorobenzene (DNFB). Unexpectedly, after treatment with DNFB, K14^Cre/+-IL-38^f/f mice were less susceptible to cutaneous inflammation of AD. Moreover, keratinocyte-specific deletion of IL-38 suppressed the migration of Langer

SUBMITTER: Yue C 

PROVIDER: S-EPMC11186352 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature