Activating as well as inhibitory circuits tightly regulate T-cell activation thresholds and effector differentiation processes enabling proper immune response outcomes. Recently, an additional molecular link between T-cell receptor signalling and CD4+ Th17 cell skewing has been reported, namely that protein kinase C (PKC) θ critically regulates Th17/Th1 phenotypic differentiation and plasticity in CD4+ T-cells by selectively acting as a ‘reprogramming element’ that suppresses Th1-typical genes during Th17-mediated immune activation in order to stabilize a Th17 cell phenotype.