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Mol Immunol. 2004 Jun;41(4):385-90.

Protein kinase C beta is dispensable for TCR-signaling.

Author information

1
Department for Medical Biology and Human Genetics, Innsbruck Medical University, Schoepfstrasse 41, A-6020 Innsbruck, Austria.

Abstract

PKCbeta has been established to be essential in B cell receptor (BCR) signaling. Additionally, a critical role of PKCbeta in TCR/CD28-stimulated regulation of IL-2 gene transcription but also exocytotic IL-2 secretion was observed in leukemic T cell lines. To now study the physiological function of PKCbeta in primary CD3(+) T cells, we used our established PKCbeta null mice. Unexpectantly, we did not reveal any defect in the development and function of T cells. Proliferative responses as well as IL-2 cytokine secretion of PKCbeta-deficient CD3(+) T cells induced by allogenic MHC, plate-bound anti-CD3 antibodies (with or without anti-CD28 costimulation), or mitogenic stimuli such as phorbol ester and Ca(2+) ionophore were comparable with wild-type controls. Thus, PKCbeta-deficient T cells had similar physiological thresholds for activation in vitro. These findings suggest that PKCbeta plays a redundant role in TCR-induced regulation of IL-2 cytokine production and T cell proliferation.

PMID:
15163535
DOI:
10.1016/j.molimm.2004.03.007
[Indexed for MEDLINE]

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