Zhaoyun Ding

Shanghai Institute of Nutrition and Health

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Yanhui Ma

Huaiyin Institute of Technology

Xinyi Qi

Peking University

Huidan Chang

Shanghai Institute of Nutrition and Health

Ju Qiu

China Agricultural University

Li Li

Chinese Academy of Sciences

Yunpeng Zhang

Changchun University of Science and Technology

Hong Zhou

Wenzhou Medical University

Ting Cai

Ningbo No. 2 Hospital

Liyun Yuan

Shanghai Institute of Nutrition and Health

Jupei Tang

Shanghai Institute of Nutrition and Health

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Shanghai Jiao Tong University

University of Chinese Academy of Sciences

Shanghai Institute of Nutrition and Health

Chinese Academy of Sciences

Shanghai Institutes for Biological Sciences

Tongren Hospital

Capital Medical University

Peking University

Northwestern University

Huaiyin Institute of Technology

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Setd2 supports GATA3+ST2+ thymic-derived Treg cells and suppresses intestinal inflammation

Nature Communications (2022)

Zhaoyun Ding Ting Cai Jupei Tang Hanxiao Sun Xinyi Qi

Treg cells acquire distinct transcriptional properties to suppress specific inflammatory responses. Transcription characteristics of Treg cells are regulated by epigenetic modifications, the mechanism of which remains obscure. Here, we report that Setd2, a histone H3K36 methyltransferase, is important for the survival and suppressive function of Treg cells, especially those from the intestine. Setd2 supports GATA3+ST2+ intestinal thymic-derived Treg (tTreg) cells by facilitating the expression and reciprocal relationship of GATA3 and ST2 in tTreg cells. IL-33 preferentially boosts Th2 cells rather than GATA3+ Treg cells in Foxp3Cre-YFPSetd2 flox/flox mice, corroborating the constraint of Th2 responses by Setd2 expression in Treg cells. SETD2 sustains GATA3 expression in human Treg cells, and SETD2 expression is increased in Treg cells from human colorectal cancer tissues. Epigenetically, Setd2 regulates the transcription of target genes (including Il1rl1) by modulating the activity of promoters and intragenic enhancers where H3K36me3 is typically deposited. Our findings provide mechanistic insights into the regulation of Treg cells and intestinal immunity by Setd2.

GATA3

10.1038/s41467-022-35250-0

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