SWI/SNF chromatin remodeling factor BAF60b restrains inflammatory diseases by affecting regulatory T cell migration.

Cell Rep

Institute of Immunology and Bone Marrow Transplantation Center, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 311100, China; Liangzhu Laboratory, Zhejiang University Medical Center, Hangzhou 311100, China; Zhejiang University School of Medicine, Hangzhou 310058, China; Laboratory Animal Center, Zhejiang University, Hangzhou 310058, China; Zhejiang University-University of Edinburgh Institute, Zhejiang University School of Medicine, Haining 314400, China; Future Health Laboratory, Innovation Center of Yangtze River Delta, Zhejiang University, Jiaxing 314100, China. Electronic address:

Published: July 2024

Regulatory T (Treg) cells play a critical regulatory role in the immune system by suppressing excessive immune responses and maintaining immune balance. The effective migration of Treg cells is crucial for controlling the development and progression of inflammatory diseases. However, the mechanisms responsible for directing Treg cells into the inflammatory tissue remain incompletely elucidated. In this study, we identified BAF60b, a subunit of switch/sucrose nonfermentable (SWI/SNF) chromatin remodeling complexes, as a positive regulator of Treg cell migration that inhibits the progression of inflammation in experimental autoimmune encephalomyelitis (EAE) and colitis animal models. Mechanistically, transcriptome and genome-wide chromatin-landscaped analyses demonstrated that BAF60b interacts with the transcription factor RUNX1 to promote the expression of CCR9 on Treg cells, which in turn affects their ability to migrate to inflammatory tissues. Our work provides insights into the essential role of BAF60b in regulating Treg cell migration and its impact on inflammatory diseases.

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Source
http://dx.doi.org/10.1016/j.celrep.2024.114458DOI Listing

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