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PMID:7650367
| Citation |
Broome, HE, Dargan, CM, Krajewski, S and Reed, JC (1995) Expression of Bcl-2, Bcl-x, and Bax after T cell activation and IL-2 withdrawal. J. Immunol. 155:2311-7 |
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| Abstract |
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. |
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| Keywords |
Animals; Apoptosis/physiology; Cell Line; DNA, Complementary/analysis; Gene Expression Regulation; Interleukin-2/physiology; Lymphocyte Activation/physiology; Mice; Mice, Inbred C57BL; Proto-Oncogene Proteins/biosynthesis; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins c-bcl-2; Spleen/cytology; T-Lymphocytes/immunology; Thymus Gland/cytology; Transfection; bcl-2-Associated X Protein; bcl-X Protein |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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