Abstract:
:CD4+ T helper (Th) differentiation is regulated by diverse inputs, including the vitamin A metabolite retinoic acid (RA). RA acts through its receptor RARα to repress transcription of inflammatory cytokines, but is also essential for Th-mediated immunity, indicating complex effects of RA on Th specification and the outcome of the immune response. We examined the impact of RA on the genome-wide transcriptional response during Th differentiation to multiple subsets. RA effects were subset-selective and were most significant in Th9 cells. RA globally antagonized Th9-promoting transcription factors and inhibited Th9 differentiation. RA directly targeted the extended Il9 locus and broadly modified the Th9 epigenome through RARα. RA-RARα activity limited murine Th9-associated pulmonary inflammation, and human allergic inflammation was associated with reduced expression of RA target genes. Thus, repression of the Th9 program is a major function of RA-RARα signaling in Th differentiation, arguing for a role for RA in interleukin 9 (IL-9) related diseases.
journal_name
Immunityjournal_title
Immunityauthors
Schwartz DM,Farley TK,Richoz N,Yao C,Shih HY,Petermann F,Zhang Y,Sun HW,Hayes E,Mikami Y,Jiang K,Davis FP,Kanno Y,Milner JD,Siegel R,Laurence A,Meylan F,O'Shea JJdoi
10.1016/j.immuni.2018.12.014subject
Has Abstractpub_date
2019-01-15 00:00:00pages
106-120.e10issue
1eissn
1074-7613issn
1097-4180pii
S1074-7613(18)30562-4journal_volume
50pub_type
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