Bcl-2 can rescue T lymphocyte development in interleukin-7 receptor-deficient mice but not in mutant rag-1(-/-) mice
- Author(s)
- Maraskovsky, E; OReilly, LA; Teepe, M; Corcoran, LM; Peschon, JJ; Strasser, A;
- Details
- Publication Year 1997-06-27,Volume 89,Issue #7,Page 1011-1019
- Journal Title
- CELL
- Publication Type
- Journal Article
- Abstract
- 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.
- Publisher
- CELL PRESS
- Keywords
- NEGATIVE SELECTION; TRANSGENIC MICE; B-CELLS; THYMOCYTE DEVELOPMENT; RAG-1-DEFICIENT MICE; V(D)J REARRANGEMENT; POSITIVE SELECTION; CONTROL POINTS; GROWTH-FACTOR; GAMMA-CHAIN
- Publisher's Version
- https://doi.org/10.1016/S0092-8674(00)80289-5
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1997-06-27 12:00:00