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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.

Original publication

DOI

10.1111/j.1600-065x.2008.00705.x

Type

Journal article

Journal

Immunological reviews

Publication Date

12/2008

Volume

226

Pages

147 - 159

Addresses

Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.

Keywords

Intestines, T-Lymphocytes, Helper-Inducer, Humans, Inflammatory Bowel Diseases, Interleukin-17, Signal Transduction, T-Lymphocytes, Regulatory, Interleukin-23