SWI/SNF chromatin remodeling factor BAF60b restrains inflammatory diseases by affecting regulatory T cell migration
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...
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Veröffentlicht in: | Cell reports (Cambridge) 2024-07, Vol.43 (7), p.114458, Article 114458 |
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Zusammenfassung: | 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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•BAF60b restrains inflammatory disease by regulating Treg cell migration•BAF60b interacts with RUNX1 for SWI/SNF-mediated chromatin remodeling•BAF60b and RUNX1 co-locate to the enhancer regions of Ccr9 in Treg cells
Liu et al. show that BAF60b is a positive regulator of Treg cell migration. They report that BAF60b interacts with RUNX1 to promote the expression of CCR9 on Treg cells, which in turn affects their ability to migrate to inflammatory tissues. |
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ISSN: | 2211-1247 2211-1247 |
DOI: | 10.1016/j.celrep.2024.114458 |