Innate immunity and intestinal microbiota in the development of Type 1 diabetes

Li Wen, Ruth E. Ley, Pavel Yu. Volchkov, Peter B. Stranges, Lia Avanesyan, Austin C. Stonebraker, Changyun Hu, F. Susan Wong, Gregory L. Szot, Jeffrey A. Bluestone, Jeffrey I. Gordon and Alexander V. Chervonsky ()
Additional contact information
Li Wen: Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
Ruth E. Ley: Center for Genome Sciences, Washington University School of Medicine, St Louis, Missouri 63108, USA
Pavel Yu. Volchkov: University of Chicago, Chicago, Illinois 60637, USA
Peter B. Stranges: University of Chicago, Chicago, Illinois 60637, USA
Lia Avanesyan: University of Chicago, Chicago, Illinois 60637, USA
Austin C. Stonebraker: The Jackson Laboratory, Bar Harbor, Maine 04609, USA
Changyun Hu: Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
F. Susan Wong: School of Medical Science, Bristol University, Bristol, BS8 1TD, UK
Gregory L. Szot: Diabetes Center at the University of California San Francisco, San Francisco, California 94143, USA
Jeffrey A. Bluestone: Diabetes Center at the University of California San Francisco, San Francisco, California 94143, USA
Jeffrey I. Gordon: Center for Genome Sciences, Washington University School of Medicine, St Louis, Missouri 63108, USA
Alexander V. Chervonsky: University of Chicago, Chicago, Illinois 60637, USA

Nature, 2008, vol. 455, issue 7216, 1109-1113

Abstract: Microbes to counter diabetes The incidence of autoimmune diabetes in NOD (non-obese diabetic) mice, a lab model for type 1 diabetes, varies depending on the conditions in which they are kept. In particular, NOD mice exposed to killed mycobacteria and other microbial products are protected against the development of diabetes, suggesting the involvement of the rapid innate immune response. Experiments in NOD mice deficient in innate immunity — through the absence of the Toll-like receptor signal adaptor protein MyD88 — now show that both innate immunity and intestinal microbiota influence predisposition to diabetes. Germ-free MyD88-negative mice developed robust diabetes, yet in mice with a complement of gut microbes similar to the normal human gut, diabetes was reduced. This raises the prospect that live 'friendly' microbes, or microbial products might be therapeutic options for type 1 diabetes.

Date: 2008
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DOI: 10.1038/nature07336

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