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 in vitro, it is reasonable to expect that Ahr would enhance Th17 cells in vivo. 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 Th17 cells. Compared to Rorc(+/+)Ahr(-/-) mice, Rorc(gfp/+)Ahr(-/-) mice had further reduced group 3 ILCs and were prone to spontaneous colitis with increased SFB and Th17 cells. Innate expression of Ahr 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.
journal_name
Immunityjournal_title
Immunityauthors
Qiu J,Guo X,Chen ZM,He L,Sonnenberg GF,Artis D,Fu YX,Zhou Ldoi
10.1016/j.immuni.2013.08.002subject
Has Abstractpub_date
2013-08-22 00:00:00pages
386-99issue
2eissn
1074-7613issn
1097-4180pii
S1074-7613(13)00330-0journal_volume
39pub_type
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