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

doi:10.1016/S1074-7613(02)00450-8

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 journal › Article › peer-review

78 Scopus citations

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 language	English (US)
Pages (from-to)	561-573
Number of pages	13
Journal	Immunity
Volume	17
Issue number	5
DOIs	https://doi.org/10.1016/S1074-7613(02)00450-8
State	Published - Nov 1 2002
Externally published	Yes

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Infectious Diseases

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10.1016/S1074-7613(02)00450-8

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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.}",

note = "Funding Information: We wish to acknowledge J. Ashwell, M.D. for his insights regarding the effects of steroids in adult mice. We are also grateful to J. Oppenheim, M.D. and W. Leonard, M.D. for their comments on the manuscript. This publication has been funded in whole or in part with Federal funds from the National Cancer Institute, National Institutes of Health, under contract No. NO1-CO-12400. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. government.",

year = "2002",

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doi = "10.1016/S1074-7613(02)00450-8",

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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.

N1 - Funding Information: We wish to acknowledge J. Ashwell, M.D. for his insights regarding the effects of steroids in adult mice. We are also grateful to J. Oppenheim, M.D. and W. Leonard, M.D. for their comments on the manuscript. This publication has been funded in whole or in part with Federal funds from the National Cancer Institute, National Institutes of Health, under contract No. NO1-CO-12400. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. government.

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.

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SN - 1074-7613

VL - 17

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JO - Immunity

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Bax deficiency partially corrects interleukin-7 receptor α deficiency

Abstract

ASJC Scopus subject areas

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