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The interleukin-23 axis in intestinal inflammation.
- Source :
-
Immunological reviews [Immunol Rev] 2008 Dec; Vol. 226, pp. 147-59. - Publication Year :
- 2008
-
Abstract
- Immune responses in the intestine are tightly regulated to ensure host protective immunity in the absence of immune pathology. Interleukin-23 (IL-23) has recently been shown to be a key player in influencing the balance between tolerance and immunity in the intestine. Production of IL-23 is enriched within the intestine and has been shown to orchestrate T-cell-dependent and T-cell-independent pathways of intestinal inflammation through effects on T-helper 1 (Th1) and Th17-associated cytokines. Furthermore, IL-23 restrains regulatory T-cell responses in the gut, favoring inflammation. Polymorphisms in the IL-23 receptor have been associated with susceptibility to inflammatory bowel diseases (IBDs) in humans, pinpointing the IL-23 axis as a key, conserved pathway in intestinal homeostasis. In addition to its role in dysregulated inflammatory responses, there is also evidence that IL-23 and the Th17 axis mediate beneficial roles in host protective immunity and barrier function in the intestine. Here we discuss the dual roles of IL-23 in intestinal immunity and how IL-23 and downstream effector pathways may make novel targets for the treatment of IBD.
- Subjects :
- Humans
Inflammatory Bowel Diseases metabolism
Interleukin-17 metabolism
Interleukin-23 metabolism
Intestinal Mucosa metabolism
Signal Transduction immunology
T-Lymphocytes, Helper-Inducer metabolism
T-Lymphocytes, Regulatory immunology
T-Lymphocytes, Regulatory metabolism
Inflammatory Bowel Diseases immunology
Interleukin-17 immunology
Interleukin-23 immunology
Intestines immunology
T-Lymphocytes, Helper-Inducer immunology
Subjects
Details
- Language :
- English
- ISSN :
- 1600-065X
- Volume :
- 226
- Database :
- MEDLINE
- Journal :
- Immunological reviews
- Publication Type :
- Academic Journal
- Accession number :
- 19161422
- Full Text :
- https://doi.org/10.1111/j.1600-065X.2008.00705.x