| First Author | Broome HE | Year | 1995 |
| Journal | J Immunol | Volume | 155 |
| Issue | 5 | Pages | 2311-7 |
| PubMed ID | 7650367 | Mgi Jnum | J:28194 |
| Mgi Id | MGI:75819 | Doi | 10.4049/jimmunol.155.5.2311 |
| Citation | Broome HE, et al. (1995) Expression of Bcl-2, Bcl-x, and Bax after T cell activation and IL-2 withdrawal. J Immunol 155(5):2311-7 |
| abstractText | Bcl-2, bcl-x, and bax genes code for proteins that affect the susceptibility of cells to apoptosis. In general, the expression of bcl-2 or bcl-x inhibits apoptosis while bax promotes apoptosis. We examined the levels of these proteins by immunoblotting in resting and activated T cells and in thymocytes. Bcl-2 and Bax proteins vary coordinately, but Bcl-x varies independently: Bcl-2 and Bax are higher in splenic T cells than in thymocytes, and their levels increase even more after T cell activation. In contrast, Bcl-x is almost undetectable in splenic T cells but is manyfold greater in thymocytes and in activated splenic T cells. When CTLL-2 cells or activated T cells are starved of IL (IL-2), the level of Bcl-x but not Bcl-2 protein drops before the onset of apoptosis. Stable transfection of either bcl-2 or bcl-x expression plasmids promotes the survival of CTLL-2 cells in the setting of IL-2 withdrawal. Over 70 to 90% of the transfected cells remain viable at 48 h after IL-2 withdrawal when all of the control transfected cells are apoptotic. These findings suggest that a decrease in Bcl-x protein levels precedes apoptosis after IL-2 withdrawal in T cells and that transfected bcl-2 promotes survival after IL-2 withdrawal by functionally masking this drop in Bcl-x. |
