| First Author | Strasser A | Year | 1994 |
| Journal | Nature | Volume | 368 |
| Issue | 6470 | Pages | 457-60 |
| PubMed ID | 8133891 | Mgi Jnum | J:17426 |
| Mgi Id | MGI:65464 | Doi | 10.1038/368457a0 |
| Citation | Strasser A, et al. (1994) Bcl-2 expression promotes B- but not T-lymphoid development in scid mice. Nature 368(6470):457-60 |
| abstractText | Expression of antigen receptors is vital for the development of B and T lymphocytes. In mice with the scid mutation, which are unable to make productive rearrangements of their immunoglobulin and T-cell receptor (TCR) genes, lymphopoiesis aborts at an early stage. The death of the immature lymphocytes by apoptosis is postulated to result from a failure to receive a survival signal induced by receptor engagement. Consistent with this hypothesis, introduction of immunoglobulin or TCR transgenes into scid mice promoted an increase in B- or T-lymphoid cells, respectively. As the protein encoded by the bcl-2 gene can inhibit cell death, we tested whether lymphopoiesis could be rescued in scid mice by crossing in a bcl-2 transgene. Strikingly, the bcl-2/scid mice accumulated almost normal numbers of B-lymphoid cells which lacked surface immunoglobulin but expressed markers of maturity. T-cell development remained blocked. Introducing a TCR transgene enabled bcl-2/scid mice to develop normal numbers of CD4+8+ thymocytes even in the absence of immunological selection, suggesting that T cells become competent to respond to bcl-2 protein only after the TCR complex is displayed at the cell surface. |
