Abstract
Abstract CD4+ T helper 17 (Th17) cells protect against pathogens at mucosal barriers by secreting cytokines that drive clearance of the pathogen by neutrophils. We found that Bcl6 interacting corepressor (BCOR) drives Th17 cell formation after Streptococcus pyogenes infection and was required for optimal expression of IL-17A and CCR6. RNA and chromatin immunoprecipitation sequencing revealed that BCOR enhances Th17 differentiation by directly repressing genes that negatively regulate Th17 cells, including genes related to the CD27 and Foxo1 signaling pathways. We have also found that Streptococcus infection generates a novel BCOR-driven Tfh-Th17 hybrid population, which may provide unique B cell help during mucosal infections. This work provides insight into a novel mechanism that enhances Th17 differentiation and function, which may be informative for the design of T cell based vaccines against extracellular pathogens at mucosal barriers.
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