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Bcl-2 family pro-apoptotic molecule, BNIP3 regulates activation-induced cell death of effector cytotoxic T lymphocytes

Wan, J. and Martinvalet, D. and Ji, X. and Lois, C. and Kaech, S. M. and Von Andrian, U. H. and Lieberman, J. and Ahmed, R. and Manjunath, N. (2003) Bcl-2 family pro-apoptotic molecule, BNIP3 regulates activation-induced cell death of effector cytotoxic T lymphocytes. Immunology, 110 (1). pp. 10-17. ISSN 0019-2805. PMCID PMC1783016. doi:10.1046/j.1365-2567.2003.01710.x.

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BNIP3 is a recently described pro‐apoptotic member of the Bcl‐2 family and in BNIP3 cDNA‐transfected cell lines, cell death occurs via a caspase‐independent pathway with opening of the mitochondrial permeability transition (PT) pore and rapid loss of mitochondrial transmembrane potential (Δψm). However, its expression or function in physiologic cell types is not known. Our results using the T‐cell receptor transgenic mice P14, specific for lymphocyte choreomeningitis virus (LCMV) glycoprotein, show that in contrast to the other Bcl‐2 family pro‐apoptotic molecules, BNIP3 is transcriptionally highly up‐regulated in effector cytotoxic T lymphocytes (CTL). Because CTL have a propensity to undergo activation‐induced cell death (AICD) upon restimulation, we tested for other features associated with BNIP3‐induced cell death. AICD of CTL was caspase‐independent as determined by measuring caspase activation during target cell killing as well as by lack of inhibition with caspase inhibitors. Moreover, similar to BNIP3‐induced cell death, CTL apoptosis was associated with increased production of reactive oxygen species and decreased Δψm. Finally, retroviral transduction of BNIP3 antisense RNA diminished AICD in effector CTL. These results suggest that BNIP3 may play an important role in T‐cell homeostasis by regulating effector CTL numbers.

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Lois, C.0000-0002-7305-2317
Additional Information:© 2003 Blackwell Publishing. Received 30 October 2002; revised 11 June 2003; accepted 19 June 2003. We thank Zhang Dong for assistance with the quantitative PCR and Premlata Shankar for critically reviewing the manuscript. This work was supported by NIH grant AI46566 to M.N.
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Issue or Number:1
PubMed Central ID:PMC1783016
Record Number:CaltechAUTHORS:20181001-113520221
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Official Citation:Wan, J. , Martinvalet, D. , Ji, X. , Lois, C. , Kaech, S. M., Von Andrian, U. H., Lieberman, J. , Ahmed, R. and Manjunath, N. (2003), The Bcl‐2 family pro‐apoptotic molecule, BNIP3 regulates activation‐induced cell death of effector cytotoxic T lymphocytes. Immunology, 110: 10-17. doi:10.1046/j.1365-2567.2003.01710.x
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:90060
Deposited By: George Porter
Deposited On:05 Oct 2018 22:59
Last Modified:16 Nov 2021 00:40

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