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    Interleukin-23 drives innate and T cell-mediated intestinal inflammation.

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    Author
    Hue, S; Ahern, P; Buonocore, S; Kullberg, MC; Cua, DJ; McKenzie, BS; Powrie, F; Maloy, KJ
    Date
    2006-10-30
    Source Title
    Journal of Experimental Medicine
    Publisher
    Rockefeller University Press
    University of Melbourne Author/s
    McKenzie, Brent
    Affiliation
    Bio21
    Metadata
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    Document Type
    Journal Article
    Citations
    Hue, S., Ahern, P., Buonocore, S., Kullberg, M. C., Cua, D. J., McKenzie, B. S., Powrie, F. & Maloy, K. J. (2006). Interleukin-23 drives innate and T cell-mediated intestinal inflammation.. J Exp Med, 203 (11), pp.2473-2483. https://doi.org/10.1084/jem.20061099.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259090
    DOI
    10.1084/jem.20061099
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118132
    Abstract
    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.

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