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Immunol Lett. 2013 Mar;151(1-2):31-8. doi: 10.1016/j.imlet.2013.02.002. Epub 2013 Feb 21.

PKCα and PKCβ cooperate functionally in CD3-induced de novo IL-2 mRNA transcription.

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Tyrolean Cancer Reserach Institute (TKFI), Austria.

Erratum in

  • Immunol Lett. 2014 Jul;160(1):104. Christina, Lutz-Nicoladoni [corrected to Lutz-Nicoladoni, Christina]; Nikolaus, Thuille [corrected to Thuille, Nikolaus]; Katarzyna, Wachowicz [corrected to Wachowicz, Katarzyna]; Thomas, Gruber [corrected to Gruber, Thomas]; Michael, Leitges [corrected to Leitges, Michael]; Gottfried, Baier [corrected to Baier, Gottfried].


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, PKCβ, has been described yet in T cell antigen receptor signalling. To investigate the hypothesis that both conventional PKCα and PKCβ isotypes may have overlapping functions in T cell activation signalling, we generated mice that lacked the genes for both isotypes. We found that PKCα(-/-)/β(-/-) 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 PKCβ converge to regulate IL-2 cytokine responses in anti-CD3 stimulated primary mouse T cells. Here, we present genetic evidence that PKCα and PKCβ cooperate in IL-2 transcriptional transactivation in primary mouse T cells independently of the actions of PKCθ.

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