Significance of the IL-23/Th17 inflammatory axis in Crohn's disease
10.3760/cma.j.cn101480-20231116-00063
- VernacularTitle:IL-23/Th17炎症轴在克罗恩病中的意义
- Author:
Ziling GOU
1
;
Yongjun WANG
;
Fanggen LU
;
Jie ZHANG
Author Information
1. 西南医科大学附属第四医院（眉山天府新区人民医院）消化内科，眉山 620564
- Publication Type:Journal Article
- Keywords:
Crohn's disease;
Interleukin 23;
T helper cell 17;
Flammatory axis;
Biologics
- From:
Chinese Journal of Inflammatory Bowel Diseases
2024;08(6):473-479
- CountryChina
- Language:Chinese
-
Abstract:
Crohn's disease (CD) is a chronic transmural inflammatory bowel disease that can affect the entire digestive tract. The etiology is unknown, but it is mainly considered to be caused by a variety of factors such as environment, genetic susceptibility, and gut microbiota, leading to immune-inflammatory reactions in the gastrointestinal mucosa. Studies have found that the interleukin 23 (IL-23) /T helper cell 17 (Th17) inflammatory axis in CD bridges innate immunity and adaptive immunity, promoting the differentiation of naive T cells into Th17 through the IL-23p19-JAK-STAT3 pathway, producing a large amount of pro-inflammatory cytokines represented by IL-17, thereby maintaining intestinal inflammation. This axis is regulated by genetic genes, gut microbiota, and bile acid metabolism. Drugs targeting some signaling molecules of the IL-23/Th17 inflammatory axis have been developed and have achieved good therapeutic effects. In the future, further development of potential target drugs for this axis will be beneficial to personalized treatment of CD.
