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Protein kinase Cε is dispensable for TCR/CD3-signaling

Protein kinase Cε is dispensable for TCR/CD3-signaling

Authors :
Gruber, Thomas
Thuille, Nikolaus
Hermann-Kleiter, Natascha
Leitges, Michael
Baier, Gottfried
Source :
Molecular Immunology. Feb2005, Vol. 42 Issue 3, p305-310. 6p.
Publication Year :
2005

Abstract

Abstract: PKCε has been strongly linked to cell activation and proliferation in many cell types, including leukemic T-cell lines. In particularly, an essential role of PKCε has been established in the IKK-β/I-κB/NF-κB transactivation cascade. To study the physiological function of PKCε in primary T-cells, we used our newly established PKCε null mice. Unexpectedly, however, we did not reveal any defect in the development and function of CD3+ T-cells. Proliferative responses as well as IL-2 cytokine secretion of PKCε-deficient 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 Ca2+ ionophore were comparable with wild-type controls. Consistently, after CD3/CD28 engagement, deficiency of PKCε did not impair NF-κB transactivation as well as CD25, CD44 and CD69 induction. Thus, PKCε-deficient T-cells had similar physiological thresholds for activation in vitro. This finding suggests that PKCε plays a redundant role in TCR-induced regulation of T-cell proliferation. [Copyright &y& Elsevier]

Details

Language :
English
ISSN :
01615890
Volume :
42
Issue :
3
Database :
Academic Search Index
Journal :
Molecular Immunology
Publication Type :
Academic Journal
Accession number :
15837943
Full Text :
https://doi.org/10.1016/j.molimm.2004.07.007