| First Author | Sentman CL | Year | 1991 |
| Journal | Cell | Volume | 67 |
| Issue | 5 | Pages | 879-88 |
| PubMed ID | 1835668 | Mgi Jnum | J:11548 |
| Mgi Id | MGI:59968 | Doi | 10.1016/0092-8674(91)90361-2 |
| Citation | Sentman CL, et al. (1991) bcl-2 inhibits multiple forms of apoptosis but not negative selection in thymocytes. Cell 67(5):879-88 |
| abstractText | The vast majority of cortical thymocytes die during T cell development while those that survive this selective process accumulate in the medulla. bcl-2, an inner mitochondrial membrane protein, has been shown to inhibit apoptosis in certain cell lines. In the thymus, bcl-2 is regionally localized to the mature T cells of the medulla. To assess the role of bcl-2 in the programmed death of thymocytes, we generated transgenic mice that redirected bcl-2 expression to cortical thymocytes. bcl-2 protected immature CD4+8+ thymocytes from glucocorticoid, radiation, and anti-CD3-induced apoptosis. Moreover, bcl-2 altered T cell maturation, resulting in increased percentages of CD3hi and CD4-8+ thymocytes. Despite this, clonal deletion of T cells that recognize endogenous superantigens still occurred. This transgenic model indicates that multiple death pathways operate within the thymus that can be distinguished by their dependence on bcl-2. |
