IL-25 contributes to development of chronic contact dermatitis in C57BL/6 mice, but not BALB/c mice

恶唑酮 免疫学 发病机制 平衡/c 免疫系统 细胞因子 特应性皮炎 白细胞介素4 医学 生物
作者
Eri Shimura,Hajime Suto,Takafumi Numata,Sachiko Yamaguchi,Kazutoshi Harada,Katsuhiko Okumura,Katsuko Sudo,Masashi Ikutani,Susumu Nakae
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier]
卷期号:628: 57-63
标识
DOI:10.1016/j.bbrc.2022.08.077
摘要

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by type 2 immune responses. Interleukin-25 (IL-25) is produced predominantly by epithelial cells. It can activate Th2 cells to produce type 2 cytokines such as IL-4, IL-5 and IL-13, contributing to host defense against nematodes. However, excessive/inappropriate production of IL-25 is considered to be involved in development of type 2 cytokine-associated allergic disorders such as asthma. On the other hand, the contribution of IL-25 to the pathogenesis of AD remains poorly understood. In the present study, we found that expression of Il25 mRNA was significantly increased in the skin of mice during oxazolone-induced chronic contact hypersensitivity (CHS), which is a mouse model of human AD. In addition, development of oxazolone-induced chronic CHS was significantly reduced in IL-25-deficient (Il25-/-) mice compared with wild-type mice on the C57BL/6, but not BALB/c, background, although IL-25 was not essential for IL-4 production by hapten-specific T cells. Therefore, IL-25 is crucial for development of chronic CHS, although that is partly dependent on the genetic background of the mice.
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