| First Author | Valenzuela JO | Year | 2005 |
| Journal | J Immunol | Volume | 174 |
| Issue | 2 | Pages | 600-4 |
| PubMed ID | 15634875 | Mgi Jnum | J:95847 |
| Mgi Id | MGI:3527395 | Doi | 10.4049/jimmunol.174.2.600 |
| Citation | Valenzuela JO, et al. (2005) Cutting edge: Bcl-3 up-regulation by signal 3 cytokine (IL-12) prolongs survival of antigen-activated CD8 T cells. J Immunol 174(2):600-4 |
| abstractText | Clonal expansion of T cells requires cell division and survival during the proliferative phase of the response. Naive murine CD8 T cells responding to Ag and costimulation undergo an abortive response characterized by impaired clonal expansion, failure to develop effector functions, and long-term tolerance. A third signal provided by IL-12 is required for full expansion, activation, and establishment of memory. The enhanced survival, and thus clonal expansion, supported by IL-12 is not due to increased Bcl-2 or Bcl-x(L) expression; both are maximally activated by signals 1 and 2. In contrast, Bcl-3, recently shown to enhance survival when ectopically expressed in T cells, is increased only when IL-12 is present. Furthermore, examination of Bcl-3-deficient CD8 T cells demonstrates that the increased survival caused by IL-12 depends upon Bcl-3. The time courses of expression suggest that Bcl-2 and Bcl-x(L) promote survival early in the response, whereas Bcl-3 acts later in the response. |
