| First Author | Thuille N | Year | 2004 |
| Journal | Mol Immunol | Volume | 41 |
| Issue | 4 | Pages | 385-90 |
| PubMed ID | 15163535 | Mgi Jnum | J:90380 |
| Mgi Id | MGI:3043441 | Doi | 10.1016/j.molimm.2004.03.007 |
| Citation | Thuille N, et al. (2004) Protein kinase C beta is dispensable for TCR-signaling. Mol Immunol 41(4):385-90 |
| abstractText | 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. |
