• Matthew R Hepworth, Thomas C Fung, Samuel H Masur, Judith R Kelsen, Fiona M McConnell, Juan Dubrot, David R Withers, Stephanie Hugues, Michael A Farrar, Walter Reith, Gérard Eberl, Robert N Baldassano, Terri M Laufer, Charles O Elson, and Gregory F Sonnenberg.
• Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Gastroenterology Division, and Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, NY, USA.
• Science. 2015 May 29;348(6238):1031-5.

AbstractInflammatory CD4(+) T cell responses to self or commensal bacteria underlie the pathogenesis of autoimmunity and inflammatory bowel disease (IBD), respectively. Although selection of self-specific T cells in the thymus limits responses to mammalian tissue antigens, the mechanisms that control selection of commensal bacteria-specific T cells remain poorly understood. Here, we demonstrate that group 3 innate lymphoid cell (ILC3)-intrinsic expression of major histocompatibility complex class II (MHCII) is regulated similarly to thymic epithelial cells and that MHCII(+) ILC3s directly induce cell death of activated commensal bacteria-specific T cells. Further, MHCII on colonic ILC3s was reduced in pediatric IBD patients. Collectively, these results define a selection pathway for commensal bacteria-specific CD4(+) T cells in the intestine and suggest that this process is dysregulated in human IBD.Copyright © 2015, American Association for the Advancement of Science.

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