Innate lymphoid cells drive interleukin-23-dependent innate intestinal pathology

Sofia Buonocore, Philip P. Ahern, Holm H. Uhlig, Ivaylo I. Ivanov, Dan R. Littman, Kevin J. Maloy () and Fiona Powrie ()
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Sofia Buonocore: Sir William Dunn School of Pathology, University of Oxford
Philip P. Ahern: Sir William Dunn School of Pathology, University of Oxford
Holm H. Uhlig: University Children’s Hospital
Ivaylo I. Ivanov: Molecular Pathogenesis Program, Howard Hughes Medical Institute, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA
Dan R. Littman: Molecular Pathogenesis Program, Howard Hughes Medical Institute, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA
Kevin J. Maloy: Sir William Dunn School of Pathology, University of Oxford
Fiona Powrie: Sir William Dunn School of Pathology, University of Oxford

Nature, 2010, vol. 464, issue 7293, 1371-1375

Abstract: Innate intestinal inflammatory responses Interleukin 23 (IL-23) has been implicated in the pathogenesis of autoimmune and chronic inflammatory disorders. New work in a mouse model has identified a previously unrecognized population of innate lymphoid cells that respond to IL-23 by inducing inflammation through the production of IL-17 and interferon-γ. Further work will be needed to establish whether this newly discovered IL-23-driven pathway contributes to chronic inflammatory diseases such as irritable bowel disease.

Date: 2010
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DOI: 10.1038/nature08949

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