IL-23 plays a key role in Helicobacter hepaticus-induced T cell-dependent colitis.

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Kullberg, MC; Jankovic, D; Feng, CG; Hue, S; Gorelick, PL; McKenzie, BS; Cua, DJ; Powrie, F; Cheever, AW; Maloy, KJ; ...Date
2006-10-30Source Title
Journal of Experimental MedicinePublisher
Rockefeller University PressUniversity of Melbourne Author/s
McKenzie, BrentAffiliation
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Kullberg, 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 Status
Open AccessOpen Access at PMC
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118119Abstract
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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