Interleukin-23 drives innate and T cell–mediated intestinal inflammation (original) (raw)
Article| October 09 2006
1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
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1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
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1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
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2Immunology and Infection Unit, Department of Biology, University of York and The Hull York Medical School, York YO10 5YW, England, UK
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3Department of Discovery Research, Schering-Plough Biopharma, Palo Alto, CA 94304
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3Department of Discovery Research, Schering-Plough Biopharma, Palo Alto, CA 94304
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1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
Search for other works by this author on:
1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
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Sophie Hue
1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
Philip Ahern
1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
Sofia Buonocore
1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
Marika C. Kullberg
2Immunology and Infection Unit, Department of Biology, University of York and The Hull York Medical School, York YO10 5YW, England, UK
Daniel J. Cua
3Department of Discovery Research, Schering-Plough Biopharma, Palo Alto, CA 94304
Brent S. McKenzie
3Department of Discovery Research, Schering-Plough Biopharma, Palo Alto, CA 94304
Fiona Powrie
1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
Kevin J. Maloy
1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
Abbreviations used: CD, Crohn's disease; IBD, inflammatory bowel disease; FSC, forward scatter; KC, mouse chemokine CXCL1; LPL, lamina propria leukocyte; MCP-1, monocyte chemoattractant protein–1; MLN, mesenteric LN; Q-PCR, quantitative PCR; SSC, side scatter.
Received: May 22 2006
Accepted: September 13 2006
Online ISSN: 1540-9538
Print ISSN: 0022-1007
The Rockefeller University Press
2006
J Exp Med (2006) 203 (11): 2473–2483.
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract involving aberrant activation of innate and adaptive immune responses. We have used two complementary models of IBD to examine the roles of interleukin (IL)-12 family cytokines in bacterially induced intestinal inflammation. Our results clearly show that IL-23, but not IL-12, is essential for the induction of chronic intestinal inflammation mediated by innate or adaptive immune mechanisms. Depletion of IL-23 was associated with decreased proinflammatory responses in the intestine but had little impact on systemic T cell inflammatory responses. These results newly identify IL-23 as a driver of innate immune pathology in the intestine and suggest that selective targeting of IL-23 represents an attractive therapeutic approach in human IBD.
The Rockefeller University Press
2006
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