The interleukin-23 axis in intestinal inflammation.

Journal article

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.

Authors: Ahern, P; Izcue, A; Maloy, K; Powrie, F

• Publication status: Published
• Journal: Immunological reviews
• Volume: 226
• Issue: 1
• Pages: 147-159
• Publication date: 2008-12-01
• DOI: 10.1111/j.1600-065x.2008.00705.x
• EISSN: 1600-065X
• ISSN: 0105-2896
• Language: English
• Keywords: T-Lymphocytes, Helper-Inducer; Humans; Interleukin-17; Interleukin-23; T-Lymphocytes, Regulatory; Signal Transduction; Inflammatory Bowel Diseases; Intestines