IL-23 plays a key role in Helicobacter hepaticus-induced T cell-dependent colitis.
AuthorKullberg, MC; Jankovic, D; Feng, CG; Hue, S; Gorelick, PL; McKenzie, BS; Cua, DJ; Powrie, F; Cheever, AW; Maloy, KJ; ...
Source TitleJournal of Experimental Medicine
PublisherRockefeller University Press
University of Melbourne Author/sMcKenzie, Brent
Document TypeJournal Article
CitationsKullberg, M. C., Jankovic, D., Feng, C. G., Hue, S., Gorelick, P. L., McKenzie, B. S., Cua, D. J., Powrie, F., Cheever, A. W., Maloy, K. J. & Sher, A. (2006). IL-23 plays a key role in Helicobacter hepaticus-induced T cell-dependent colitis.. J Exp Med, 203 (11), pp.2485-2494. https://doi.org/10.1084/jem.20061082.
Access StatusOpen Access
Open Access at PMChttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118119
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract that is caused in part by a dysregulated immune response to the intestinal flora. The common interleukin (IL)-12/IL-23p40 subunit is thought to be critical for the pathogenesis of IBD. We have analyzed the role of IL-12 versus IL-23 in two models of Helicobacter hepaticus-triggered T cell-dependent colitis, one involving anti-IL-10R monoclonal antibody treatment of infected T cell-sufficient hosts, and the other involving CD4+ T cell transfer into infected Rag-/- recipients. Our data demonstrate that IL-23 and not IL-12 is essential for the development of maximal intestinal disease. Although IL-23 has been implicated in the differentiation of IL-17-producing CD4+ T cells that alone are sufficient to induce autoimmune tissue reactivity, our results instead support a model in which IL-23 drives both interferon gamma and IL-17 responses that together synergize to trigger severe intestinal inflammation.
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