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Bax deficiency partially corrects interleukin-7 receptor alpha deficiency

  1. Author:
    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.

  2. Author Address

    NCI, Mol Immunoregulat Lab, Canc Res Ctr, Frederick, MD 21702 USA NCI, Mol Immunoregulat Lab, Canc Res Ctr, Frederick, MD 21702 USA NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA Univ Miami, Dept Pathol, Miami, FL 33136 USA SAIC Frederick, Intramural Res Support Program, Frederick, MD 21702 USA NCI, Expt Immunol Lab, Canc Res Ctr, Frederick, MD 21702 USA Durum SK NCI, Mol Immunoregulat Lab, Canc Res Ctr, Frederick, MD 21702 USA
    1. Year: 2002
  2. Journal: Immunity
    1. 17
    2. 5
    3. Pages: 561-573
  4. Type of Article: Article
  1. 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 a chain (IL-7R). Starting at birth, we observed complete recovery of all stages of (3 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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