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 0022-1007Full text not available from this repository.
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.
|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|
|Publisher:||Rockefeller University Press|