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 journalArticle

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
Externally publishedYes

Fingerprint

Interleukin-7 Receptors
Interleukin-7
bcl-Associated Death Protein
Cytoprotection
Hematopoiesis
Thymocytes
Parturition
Apoptosis
Cytokines
T-Lymphocytes
Proteins

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases
  • Immunology

Cite this

Khaled, A. R., Li, W. Q., Huang, J., Fry, T. J., Khaled, A. S., Mackall, C. L., ... Durum, S. K. (2002). Bax deficiency partially corrects interleukin-7 receptor α deficiency. Immunity, 17(5), 561-573. https://doi.org/10.1016/S1074-7613(02)00450-8

Bax deficiency partially corrects interleukin-7 receptor α deficiency. / Khaled, Annette R.; Li, Wen Qing; Huang, Jiaqiang; Fry, Terry J.; Khaled, Amr S.; Mackall, Crystal L.; Muegge, Kathrin; Young, Howard A.; Durum, Scott K.

In: Immunity, Vol. 17, No. 5, 01.11.2002, p. 561-573.

Research output: Contribution to journalArticle

Khaled, AR, Li, WQ, Huang, J, Fry, TJ, Khaled, AS, Mackall, CL, Muegge, K, Young, HA & Durum, SK 2002, 'Bax deficiency partially corrects interleukin-7 receptor α deficiency', Immunity, vol. 17, no. 5, pp. 561-573. https://doi.org/10.1016/S1074-7613(02)00450-8
Khaled AR, Li WQ, Huang J, Fry TJ, Khaled AS, Mackall CL et al. Bax deficiency partially corrects interleukin-7 receptor α deficiency. Immunity. 2002 Nov 1;17(5):561-573. https://doi.org/10.1016/S1074-7613(02)00450-8
Khaled, Annette R. ; Li, Wen Qing ; Huang, Jiaqiang ; Fry, Terry J. ; Khaled, Amr S. ; Mackall, Crystal L. ; Muegge, Kathrin ; Young, Howard A. ; Durum, Scott K. / Bax deficiency partially corrects interleukin-7 receptor α deficiency. In: Immunity. 2002 ; Vol. 17, No. 5. pp. 561-573.
@article{509da0ffb99f4b65be9bcea54aaaea58,
title = "Bax deficiency partially corrects interleukin-7 receptor α deficiency",
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.",
author = "Khaled, {Annette R.} and Li, {Wen Qing} and Jiaqiang Huang and Fry, {Terry J.} and Khaled, {Amr S.} and Mackall, {Crystal L.} and Kathrin Muegge and Young, {Howard A.} and Durum, {Scott K.}",
year = "2002",
month = "11",
day = "1",
doi = "10.1016/S1074-7613(02)00450-8",
language = "English (US)",
volume = "17",
pages = "561--573",
journal = "Immunity",
issn = "1074-7613",
publisher = "Cell Press",
number = "5",

}

TY - JOUR

T1 - Bax deficiency partially corrects interleukin-7 receptor α deficiency

AU - Khaled, Annette R.

AU - Li, Wen Qing

AU - Huang, Jiaqiang

AU - Fry, Terry J.

AU - Khaled, Amr S.

AU - Mackall, Crystal L.

AU - Muegge, Kathrin

AU - Young, Howard A.

AU - Durum, Scott K.

PY - 2002/11/1

Y1 - 2002/11/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0036849781&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036849781&partnerID=8YFLogxK

U2 - 10.1016/S1074-7613(02)00450-8

DO - 10.1016/S1074-7613(02)00450-8

M3 - Article

VL - 17

SP - 561

EP - 573

JO - Immunity

JF - Immunity

SN - 1074-7613

IS - 5

ER -