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Bax deficiency partially corrects interleukin-7 receptor alpha deficiency

Annette R Khaled1, Wen Qing Li, Jiaqiang Huang

  • 1Laboratory of Molecular Immunoregulation, Center for Cancer Research, National Cancer Institute - Frederick, MD 21702, USA.

Immunity
|November 16, 2002
PubMed

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.

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