Bax deficiency partially corrects interleukin-7 receptor α deficiency

Annette R. Khaled, Wen Qing Li, Jiaqiang Huang, Terry J. Fry, Amr S. Khaled, Crystal L. Mackall, Kathrin Muegge, Howard A. Young, Scott K. Durum

Research output: Contribution to journalArticlepeer-review

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 α chain (IL-7R). Starting at birth, we observed complete recovery of all stages of αβ 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.

Original languageEnglish (US)
Pages (from-to)561-573
Number of pages13
JournalImmunity
Volume17
Issue number5
DOIs
StatePublished - Nov 1 2002

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Fingerprint Dive into the research topics of 'Bax deficiency partially corrects interleukin-7 receptor α deficiency'. Together they form a unique fingerprint.

Cite this