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- W2462183776 abstract "Abstract Foxp3+ regulatory T cells are crucial for peripheral tolerance and immune homeostasis. During inflammation, the steady expression of Foxp3 in mature regulatory T cells is essential for maintenance of their lineage identity and suppressive function. However, the molecular machinery governing regulatory T cells’ resilience to inflammation induced Foxp3 destabilization is not fully understood. Here, we demonstrate that Methyl-CpG binding protein 2, an eminent epigenetic regulator known primarily as the etiological factor of the neurological disorder Rett syndrome, is essential to sustain regulatory T cells’ Foxp3 expression during inflammation. In response to inflammatory stimuli, Methyl-CpG binding protein 2 is specifically recruited to the CNS2 region of the foxp3 locus, where it collaborates with CAMP responsive element binding protein 1 to promote local histone H3 acetylation, thereby counteracting inflammation induced epigenetic silencing of foxp3. Consequently, regulatory T cell specific deletion of Methyl-CpG binding protein 2 is sufficient to induce spontaneous immune activation in young adult mice. Furthermore, we demonstrate that Foxp3 expression diminishes with time in Methyl-CpG binding protein 2 deficient regulatory T cells, resulting in their failure to suppress Th17-mediated colitis. Thus, Methyl-CpG binding protein 2 serves as a critical safeguard that confers regulatory T cells with resilience against inflammation." @default.
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- W2462183776 date "2013-05-01" @default.
- W2462183776 modified "2023-09-25" @default.
- W2462183776 title "MeCP2 enforces Foxp3 expression to determine natural regulatory T cells’ resilience to inflammation (P1023)" @default.
- W2462183776 doi "https://doi.org/10.4049/jimmunol.190.supp.139.1" @default.
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