Group 3 innate lymphoid cells inhibit T-cell-mediated intestinal inflammation through aryl hydrocarbon receptor signaling and regulation of microflora

Ju Qiu, Xiaohuan Guo, Zong ming E. Chen, Lei He, Gregory F. Sonnenberg, David Artis, Yang Xin Fu, Liang Zhou

Research output: Contribution to journalArticle

222 Scopus citations

Abstract

Aryl hydrocarbon receptor (Ahr) is crucial for the maintenance and function of group 3 innate lymphoid cells (ILCs), which are important in gut immunity. Because Ahr promotes T helper 17 (Th17) cell differentiation invitro, it is reasonable to expect that Ahr would enhance Th17 cells invivo. Instead, we show that Ahr deficiency caused increased intestinal Th17 cells, raising the possibility that group 3 ILCs could negatively regulate Th17 cells. Reduced innate interleukin-22 (IL-22) in Ahr-deficient mice allowed expansion of commensal segmented filamentous bacteria (SFB), known to promote Th17cells. Compared to Rorc+/+Ahr-/- mice, Rorcgfp/+Ahr-/- mice had further reduced group 3ILCs and were prone to spontaneous colitis with increased SFB and Th17 cells. Innate expression ofAhr played a protective role in T-cell-mediated experimental colitis by suppressing pathogenic Th17 cells. Our data reveal an intricate balance between ILCs and Th17 cells regulated by Ahr and commensal flora.

Original languageEnglish (US)
Pages (from-to)386-399
Number of pages14
JournalImmunity
Volume39
Issue number2
DOIs
StatePublished - Aug 22 2013

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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