Impact of RORgt in regulating CD4 T cells primed under Th17 conditions

CD4 T cells are an essential component of antiviral adaptive immune cell responses. Central to the functional capabilities of CD4 T Cells is their ability to differentiate into distinct subsets. Subset differentiation and maintenance is dependent on the coordinated and sequential activation of certain master regulator transcription factors. While antiviral responses are predominantly Th1, prior studies have shown that both T-bet and Eomes, two critical regulators of Th1 responses are dispensable for CD4 T cell mediated protection. CD4 T Cells lacking both T-bet and Eomes produce strong and highly protective Th17 response characterized by high expression of the transcription factor RORγt. Here we determine the impact of RORγt regulation in CD4 T Cells primed under Th17 conditions and also deficient in T-bet and Eomes. Our studies reveal RORγt regulates several hundred genes that in Th17 CD4 T Cells, thus providing a potential molecular framework for targeting protective anti-viral immunity. RNA-seq profiling and comparison of day 4 CD4 T cells primed under Th17 condiitions and lacking either T-bet and Eomes or T-bet, Eomes and RORγt