ABSTRACT
The physiological functions of PKCα and PKCθ isotypes downstream of the antigen receptor have been defined in CD3(+) T cells. In contrast, no function of the second conventional PKC member, PKCß, has been described yet in T cell antigen receptor signalling. To investigate the hypothesis that both conventional PKCα and PKCß isotypes may have overlapping functions in T cell activation signalling, we generated mice that lacked the genes for both isotypes. We found that PKCα(-/-)/ß(-/-) animals are viable, live normal life spans and display normal T cell development. However, these animals possess additive defects in T cell responses in comparison to animals that carry single mutations in these genes. Our studies demonstrate that the activities of PKCα and PKCß converge to regulate IL-2 cytokine responses in anti-CD3 stimulated primary mouse T cells. Here, we present genetic evidence that PKCα and PKCß cooperate in IL-2 transcriptional transactivation in primary mouse T cells independently of the actions of PKCθ.
