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

  1. Author:
    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.

  2. Author Address

    NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA. Univ York, Dept Biol, Immunol & Infect Unit, York YO10 5YW, N Yorkshire, England. Hull York Med Sch, York YO10 5YW, N Yorkshire, England. Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England. Sci Applicat Int Corp, FCRDC, NCI,Lab Anim Sci Program, Anim Hlth Diagnost Lab, Frederick, MD 21702 USA. Schering Plough Biopharma, Dept Discovery Res, Palo Alto, CA 94304 USA. Biomed Res Inst, Rockville, MD 20852 USA.;Kullberg, MC, NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.;mk512@york.ac.uk
    1. Year: 2006
    2. Date: Oct
  2. Journal: Journal of Experimental Medicine
    1. 203
    2. 11
    3. Pages: 2485-2494
  4. Type of Article: Article
  5. ISSN: 0022-1007
  1. 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 gamma and IL-17 responses that together synergize to trigger severe intestinal inflammation.

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External Sources

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  2. DOI: 10.1084/jem.20061082
  3. View record in Web of Science®
  4. WOS: 000241670800013

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