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

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. (2006) IL-23 plays a key role in Helicobacter hepaticus-induced T cell-dependent colitis. Journal of Experimental Medicine, 203 (11). pp. 2485-2494. ISSN 0022-1007

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Abstract

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 and IL-17 responses that together synergize to trigger severe intestinal inflammation.

Item Type: Article
Institution: The University of York
Academic Units: The University of York > Biology (York)
The University of York > Hull York Medical School (York)
Depositing User: York RAE Import
Date Deposited: 04 Jun 2009 08:32
Last Modified: 04 Jun 2009 08:32
Published Version: http://dx.doi.org/10.1084/jem.20061082
Status: Published
Publisher: Rockefeller University Press
Identification Number: 10.1084/jem.20061082
URI: http://eprints.whiterose.ac.uk/id/eprint/6650

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