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  Protein kinase C beta is dispensable for TCR-signaling.

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.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0012-ED3C-6 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0027-DAB9-A
Genre: Journal Article

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 Creators:
Thuille, N., Author
Gruber, T., Author
Bock, G., Author
Leitges, M.1, Author              
Baier, G., Author
Affiliations:
1Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society, ou_persistent34              

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Free keywords: Animals; Antigens, CD28/immunology; Cell Division; Genes, Reporter; Humans; Interleukin-2/genetics/secretion; Ionomycin/pharmacology; Ionophores/pharmacology; Isoenzymes/genetics/physiology; Jurkat Cells; Luciferases/biosynthesis/genetics; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Mice, Knockout; Muromonab-CD3/pharmacology; Phorbol 12,13-Dibutyrate/pharmacology; Promoter Regions (Genetics)/genetics; Protein Kinase C/deficiency/genetics/*physiology; Receptors, Antigen, T-Cell/physiology; Recombinant Fusion Proteins/physiology; Research Support, Non-U.S. Gov't; Signal Transduction; T-Lymphocytes/enzymology/immunology; Transfection
 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.

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 Dates: 2004-06
 Publication Status: Published in print
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Title: Molecular Immunology
Source Genre: Journal
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Pages: - Volume / Issue: 41 (4) Sequence Number: - Start / End Page: 385 - 390 Identifier: -