| First Author | Gruber T | Year | 2005 |
| Journal | Mol Immunol | Volume | 42 |
| Issue | 3 | Pages | 305-10 |
| PubMed ID | 15589318 | Mgi Jnum | J:94663 |
| Mgi Id | MGI:3513657 | Doi | 10.1016/j.molimm.2004.07.007 |
| Citation | Gruber T, et al. (2005) Protein kinase Cvarepsilon is dispensable for TCR/CD3-signaling. Mol Immunol 42(3):305-310 |
| abstractText | PKCvarepsilon has been strongly linked to cell activation and proliferation in many cell types, including leukemic T-cell lines. In particularly, an essential role of PKCvarepsilon has been established in the IKK-beta/I-kappaB/NF-kappaB transactivation cascade. To study the physiological function of PKCvarepsilon in primary T-cells, we used our newly established PKCvarepsilon 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 PKCvarepsilon-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 Ca(2+) ionophore were comparable with wild-type controls. Consistently, after CD3/CD28 engagement, deficiency of PKCvarepsilon did not impair NF-kappaB transactivation as well as CD25, CD44 and CD69 induction. Thus, PKCvarepsilon-deficient T-cells had similar physiological thresholds for activation in vitro. This finding suggests that PKCvarepsilon plays a redundant role in TCR-induced regulation of T-cell proliferation. |
