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Journal Article

Protein kinase C beta is dispensable for TCR-signaling.

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Leitges,  M.
Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society;

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Citation

Thuille, N., Gruber, T., Bock, G., Leitges, M., & Baier, G. (2004). Protein kinase C beta is dispensable for TCR-signaling. Molecular Immunology, 41(4), 385-390. Retrieved from http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15163535.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0012-ED3C-6
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.