TY - JOUR
T1 - Bcl-2 rescues T lymphopoiesis in Interleukin-7 receptor-deficient mice
AU - Akashi, Koichi
AU - Kondo, Motonari
AU - Von Freeden-Jeffry, Ursula
AU - Murray, Richard
AU - Weissman, Irving L.
N1 - Funding Information:
Correspondence should be addressed to K. A. (Akashi@Darwin. Stanford.edu). We are indebted to Dr. S. Nishikawa for A7R34, Drs. M. Grusby and L. H. Glimcher for MHC −/− mice, and Dr. S. Cory for Eμ- bcl-2 transgenic mice. The DNAX Research Institute of Molecular and Cellular Biology is supported by Schering-Plough Corporation. This work was mainly supported by National Cancer Institute grant CA42551 to I. L. W., and in part by a grant from Uehara Memorial Foundation to K. A.
PY - 1997
Y1 - 1997
N2 - Mice lacking functional IL-7 or IL-7Rα genes are severely deficient in developing thymocytes, T cells, and B cells. IL-7 and IL-7 receptor functions are believed to result in lymphoid cell proliferation and cell maturation, implying signal transduction pathways directly involved in mitogenesis and elaboration of developmentally specific new gene programs. Here, we show that enforced expression of the bcl-2 gene in T-lymphoid cells (by crossing in the Eμ-bcl-2 transgene) in IL-7Rα-deficient mice results in a significant restoration of thymic positive selection and T cell numbers and function. We propose cell survival signals to be the principal function of IL-7R engagement in thymic and T cell development.
AB - Mice lacking functional IL-7 or IL-7Rα genes are severely deficient in developing thymocytes, T cells, and B cells. IL-7 and IL-7 receptor functions are believed to result in lymphoid cell proliferation and cell maturation, implying signal transduction pathways directly involved in mitogenesis and elaboration of developmentally specific new gene programs. Here, we show that enforced expression of the bcl-2 gene in T-lymphoid cells (by crossing in the Eμ-bcl-2 transgene) in IL-7Rα-deficient mice results in a significant restoration of thymic positive selection and T cell numbers and function. We propose cell survival signals to be the principal function of IL-7R engagement in thymic and T cell development.
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U2 - 10.1016/S0092-8674(00)80291-3
DO - 10.1016/S0092-8674(00)80291-3
M3 - Article
C2 - 9215626
AN - SCOPUS:0031587826
SN - 0092-8674
VL - 89
SP - 1033
EP - 1041
JO - Cell
JF - Cell
IS - 7
ER -