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

Kullberg, M. C. et al. (2006) IL-23 plays a key role in Helicobacter hepaticus-induced T cell-dependent colitis. Journal of Experimental Medicine, 203(11), pp. 2485-2494. (doi: 10.1084/jem.20061082) (PMID:17030948) (PMCID:PMC2118119)

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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.

Item Type:Articles
Glasgow Author(s) Enlighten ID:Maloy, Professor Kevin
Authors: 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., and Sher, A.
College/School:College of Medical Veterinary and Life Sciences > School of Infection & Immunity
Journal Name:Journal of Experimental Medicine
Publisher:Rockefeller University Press
ISSN (Online):1540-9538
Published Online:09 October 2006

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