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Bax deficiency partially corrects interleukin-7 receptor alpha deficiency IMMUNITY Khaled, A. R., Li, W. Q., Huang, J. Q., Fry, T. J., Khaled, A. S., Mackall, C. L., Muegge, K., Young, H. A., Durum, S. K. 2002; 17 (5): 561-573

Abstract

The requirement for cytokines in hematopoiesis is partly attributable to the protection of cells from apoptosis. Since IL-7 is required for normal T cell development, we evaluated the role of Bax in vivo by generating mice deficient in both Bax and the IL-7 receptor alpha chain (IL-7R). Starting at birth, we observed complete recovery of all stages of alphabeta thymocyte development up to 4 weeks of age. However, by 12 weeks of age, thymic cellularity had reverted to that of mice deficient in IL-7R alone. The BH3 only proteins, Bad and Bim, were also part of the death pathway repressed by IL-7. Thus, in young mice, Bax emerges as an essential protein in the death pathway induced by IL-7 deficiency.

View details for Web of Science ID 000179335100003

View details for PubMedID 12433363