| First Author | Maraskovsky E | Year | 1997 |
| Journal | Cell | Volume | 89 |
| Issue | 7 | Pages | 1011-9 |
| PubMed ID | 9215624 | Mgi Jnum | J:41239 |
| Mgi Id | MGI:893318 | Doi | 10.1016/s0092-8674(00)80289-5 |
| Citation | Maraskovsky E, et al. (1997) Bcl-2 can rescue T lymphocyte development in interleukin-7 receptor-deficient mice but not in mutant rag-1-/- mice. Cell 89(7):1011-9 |
| abstractText | Signals from cytokine and antigen receptors play crucial roles during lymphocyte development. Mice lacking interleukin-7 receptor are lymphopenic, due to a defect in cell expansion at an early stage of differentiation, and the few mature T cells that develop in IL-7R-/- animals are functionally impaired. Both defects were rescued completely by overexpression of the anti-apoptosis protein Bcl-2. T cell progenitors lacking antigen receptor molecules are also blocked in differentiation and die, presumably because they fail to receive a positive signal via their pre-T cell receptor. Surprisingly, Bcl-2 did not promote survival or differentiation of T cells in rag-1-/- mice. These results provide evidence that blocking apoptosis is the essential function of IL-7R during differentiation and activation of T lymphocytes and that pre-TCR signaling blocks a pathway to apoptosis that is insensitive to Bcl-2. |
