The transcriptional regulator Sin3A balances IL-17A and Foxp3 expression in primary CD4 T cells

ABSTRACT: The Sin3 transcriptional regulator homolog A (Sin3A) is the core member of a multi-protein chromatin-modifying complex. Its inactivation at the CD4/CD8 double-negative stage halts further thymocyte development. Among various functions, Sin3A regulates STAT3 transcriptional activity, central to the differentiation of Th17 cells active in inflammatory disorders and opportunistic infections. To further investigate the consequences of conditional Sin3A inactivation in more mature precursors and post-thymic T cell, we have generated CD4-Cre and CD4-CreERT2 Sin3AF/F mice. Sin3A inactivation in vivo hinder both thymocyte development, and peripheral T cell survival. In vitro, in Th17 skewing conditions, Sin3A deficient cells proliferate and acquire memory markers and yet fail to properly upregula

SUBMITTER: Laura Perucho Aznar 

PROVIDER: S-SCDT-10_15252-EMBR_202255326 | biostudies-other |

REPOSITORIES: biostudies-other