Kullberg, M.C., Jankovic, D., Feng, C.G. et al. (8 more authors) (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
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.
Metadata
Item Type: | Article |
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Authors/Creators: |
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Dates: |
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Institution: | The University of York |
Academic Units: | The University of York > Faculty of Sciences (York) > Biology (York) The University of York > Faculty of Sciences (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 |
Open Archives Initiative ID (OAI ID): | oai:eprints.whiterose.ac.uk:6650 |