Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 628, Issue -, Pages 57-63Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2022.08.077
Keywords
Allergy; Contact hypersensitivity; Atopic dermatitis; Interleukin-25; Mouse model
Categories
Funding
- Japan Society for the Promotion of Science [21790942, 21H02963, 24688029]
- Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency [JPMJPR18H6]
Ask authors/readers for more resources
Atopic dermatitis (AD) is a chronic inflammatory skin disease with unclear pathogenesis. The study found that the expression of interleukin-25 (IL-25) was significantly increased in a mouse model of oxazolone-induced chronic contact hypersensitivity (CHS), which is similar to human AD. IL-25 plays a crucial role in the development of chronic CHS, although it depends on the genetic background of the mice to some extent.
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 oxazoloneinduced chronic CHS was significantly reduced in IL-25-deficient (Il25-/-) mice compared with wildtype 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.(c) 2022 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available