IL-23 plays a key role in Helicobacter hepaticus–induced T cell–dependent colitis (original) (raw)
Article| October 09 2006
1Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892
2Immunology and Infection Unit, Department of Biology, University of York and The Hull York Medical School, York YO10 5YW, UK
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1Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892
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1Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892
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3Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK
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4Animal Health Diagnostic Laboratory, Laboratory Animal Sciences Program, National Cancer Institute-FCRDC, Science Applications International Corporation, Frederick, MD 21702
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5Department of Discovery Research, Schering-Plough Biopharma, Palo Alto, CA 94304
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5Department of Discovery Research, Schering-Plough Biopharma, Palo Alto, CA 94304
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3Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK
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6The Biomedical Research Institute, Rockville, MD 20852
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3Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK
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1Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892
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Marika C. Kullberg
1Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892
2Immunology and Infection Unit, Department of Biology, University of York and The Hull York Medical School, York YO10 5YW, UK
Dragana Jankovic
1Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892
Carl G. Feng
1Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892
Sophie Hue
3Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK
Peter L. Gorelick
4Animal Health Diagnostic Laboratory, Laboratory Animal Sciences Program, National Cancer Institute-FCRDC, Science Applications International Corporation, Frederick, MD 21702
Brent S. McKenzie
5Department of Discovery Research, Schering-Plough Biopharma, Palo Alto, CA 94304
Daniel J. Cua
5Department of Discovery Research, Schering-Plough Biopharma, Palo Alto, CA 94304
Fiona Powrie
3Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK
Allen W. Cheever
6The Biomedical Research Institute, Rockville, MD 20852
Kevin J. Maloy
3Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK
Alan Sher
1Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892
Abbreviations used: CIA, collagen-induced arthritis; EAE, experimental autoimmune encephalomyelitis; Hh+, _H. hepaticus_–infected; IBD, inflammatory bowel disease; MLN, mesenteric lymph node; SHelAg, soluble H. hepaticus antigen.
K.J. Maloy and A. Sher contributed equally to this work.
Received: May 22 2006
Accepted: September 15 2006
Online ISSN: 1540-9538
Print ISSN: 0022-1007
The Rockefeller University Press
2006
J Exp Med (2006) 203 (11): 2485–2494.
Citation
Marika C. Kullberg, Dragana Jankovic, Carl G. Feng, Sophie Hue, Peter L. Gorelick, Brent S. McKenzie, Daniel J. Cua, Fiona Powrie, Allen W. Cheever, Kevin J. Maloy, Alan Sher; IL-23 plays a key role in _Helicobacter hepaticus_–induced T cell–dependent colitis . _J Exp Med 30 October 2006; 203 (11): 2485–2494. doi: https://doi.org/10.1084/jem.20061082
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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 γ and IL-17 responses that together synergize to trigger severe intestinal inflammation.
The Rockefeller University Press
2006
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