| First Author | Shimura E | Year | 2022 |
| Journal | Biochem Biophys Res Commun | Volume | 628 |
| Pages | 57-63 | PubMed ID | 36081279 |
| Mgi Jnum | J:328534 | Mgi Id | MGI:7336420 |
| Doi | 10.1016/j.bbrc.2022.08.077 | Citation | Shimura E, et al. (2022) IL-25 contributes to development of chronic contact dermatitis in C57BL/6 mice, but not BALB/c mice. Biochem Biophys Res Commun 628:57-63 |
| abstractText | 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. |
