| Literature DB >> 36165199 |
Leon Friesen1,2, Raymond Kostlan2, Qingyang Liu1,2, Hao Yu3, Jinfang Zhu4, Nicholas Lukacs1,2, Chang H Kim5,2,6.
Abstract
IL-9, produced mainly by specialized T cells, mast cells, and group 2 innate lymphoid cells, regulates immune responses, including anti-helminth and allergic responses. Polarization of naive CD4 T cells into IL-9-producing T cells (Th9s) is induced by IL-4 and TGF-β1 or IL-1β. In this article, we report that the transcription factor growth factor-independent 1 transcriptional repressor (GFI1) plays a negative role in mouse Th9 polarization. Moreover, the expression of GFI1 is controlled by liganded RARα, allowing GFI1 to mediate the negative effect of retinoic acid on IL-9 expression. The Gfi1 gene has multiple RARα binding sites in the promoter region for recruiting nuclear coactivator steroid receptor coactivator-3 and p300 for histone epigenetic modifications in a retinoic acid-dependent manner. Retinoic acid-induced GFI1 binds the Il9 gene and suppresses its expression. Thus, GFI1 is a novel negative regulator of Il9 gene expression. The negative GFI1 pathway for IL-9 regulation provides a potential control point for Th9 activity.Entities:
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Year: 2022 PMID： 36165199 PMCID： PMC9522314 DOI： 10.4049/jimmunol.2200328
Source DB: PubMed Journal: J Immunol ISSN： 0022-1767 Impact factor: 5.426