| First Author | Saibil SD | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 5 | Pages | 2932-9 |
| PubMed ID | 17312138 | Mgi Jnum | J:144106 |
| Mgi Id | MGI:3830128 | Doi | 10.4049/jimmunol.178.5.2932 |
| Citation | Saibil SD, et al. (2007) CD4+ and CD8+ T cell survival is regulated differentially by protein kinase Ctheta, c-Rel, and protein kinase B. J Immunol 178(5):2932-9 |
| abstractText | An effective immune response requires the expansion and survival of a large number of activated T cells. This study compared the role of protein kinase C (PKC)theta and associated signaling molecules in the survival of activated primary CD4+ vs CD8+ murine T cells. We demonstrate that the absence of PKCtheta resulted in a moderate survival defect in CD4+ T cells and a striking survival defect of CD8+ T lymphocytes. CD8+ T cells lacking the c-Rel, but not the NF-kappaB1/p50, member of the NF-kappaB family of transcription factors displayed a similar impairment in cell survival as PKCtheta(-/-) CD8(+) T lymphocytes. This implicates c-Rel as a key target of PKCtheta-mediated survival signals in CD8+ T cells. In addition, both c-Rel(-/-) and PKCtheta(-/-) T cells also displayed impaired expression of the antiapoptotic Bcl-x(L) protein upon activation. Changes in Bcl-x(L) expression, however, did not correlate with the survival of CD4+ or CD8+ lymphocytes. The addition of protein kinase B-mediated survival signals could restore partially CD4+ T cell viability, but did not dramatically influence CD8+ survival. Active protein kinase B was also unable to restore proliferative responses in CD8+ PKCtheta(-/-) T cells. The survival of CD4+ and CD8+ T cells deficient in either PKCtheta or c-Rel, however, was promoted by the addition of IL-2. Collectively, these data demonstrate that CD4+ and CD8+ T cell survival signals are differentially programmed. |
