| First Author | Gonzalez J | Year | 2003 |
| Journal | Blood | Volume | 101 |
| Issue | 7 | Pages | 2679-85 |
| PubMed ID | 12406903 | Mgi Jnum | J:128822 |
| Mgi Id | MGI:3768054 | Doi | 10.1182/blood-2002-04-1229 |
| Citation | Gonzalez J, et al. (2003) A1 is a growth-permissive antiapoptotic factor mediating postactivation survival in T cells. Blood 101(7):2679-85 |
| abstractText | The regulation of cell death in activated naive T cells is not well understood. We examined the expression of A1, an antiapoptotic member of the Bcl-2 family, following activation of naive mouse splenocytes. A1 gene expression was strongly but transiently induced during the first day of activation, with a peak at 2 to 6 hours, whereas Bcl-2 mRNA was simultaneously transiently down-regulated. Transgenic (Tg) overexpression of A1-a in T cells via the lck distal promoter resulted in decreased apoptosis following activation either with concanavalin A or with antibodies to CD3 and CD28 and led to a doubling of T-cell yield by 5 days. Tg A1-a also partially protected thymocytes from several proapoptotic stimuli but did not protect T-cell blasts from cell death induced by reactivation via the T-cell receptor. Tg Bcl-2 and Tg A1-a showed a similar ability to reduce apoptosis in both resting and activated T cells. However, in activated splenocyte cultures, the increase in 5-day T-cell yield observed with Tg Bcl-2 was only half that produced by Tg A1-a. This difference could be attributed at least in part to the fact that A1, unlike Bcl-2, did not inhibit S-phase entry of activated cells. The A1 protein may represent an adaptation of the Bcl-2 gene family to the need for survival regulation in the context of a proliferative stimulus. |
