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Published 3 January 2006. doi:10.1083/jcb.200506189
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 172, Number 1, 127-137
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Article

 Bcl-2 differentially regulates Ca2+ signals according to the strength of T cell receptor activation

Fei Zhong1, Michael C. Davis1,2, Karen S. McColl1, and Clark W. Distelhorst1,2,3,4

1 Department of Medicine, Case Western Reserve University
2 Department of Pharmacology, Case Western Reserve University
3 Comprehensive Cancer Center, Case Western Reserve University
4 University Hospitals of Cleveland, Cleveland, OH 44106

Correspondence to Clark W. Distelhorst: cwd{at}case.edu

To investigate the effect of Bcl-2 on Ca2+ signaling in T cells, we continuously monitored Ca2+ concentration in Bcl-2–positive and –negative clones of the WEHI7.2 T cell line after T cell receptor (TCR) activation by anti-CD3 antibody. In Bcl-2–negative cells, high concentrations of anti-CD3 antibody induced a transient Ca2+ elevation, triggering apoptosis. In contrast, low concentrations of anti-CD3 antibody induced Ca2+ oscillations, activating the nuclear factor of activated T cells (NFAT), a prosurvival transcription factor. Bcl-2 blocked the transient Ca2+ elevation induced by high anti-CD3, thereby inhibiting apoptosis, but did not inhibit Ca2+ oscillations and NFAT activation induced by low anti-CD3. Reduction in the level of all three inositol 1,4,5-trisphosphate (InsP3) receptor subtypes by small interfering RNA inhibited the Ca2+ elevation induced by high but not low anti-CD3, suggesting that Ca2+ responses to high and low anti-CD3 may have different requirements for the InsP3 receptor. Therefore, Bcl-2 selectively inhibits proapoptotic Ca2+ elevation induced by strong TCR activation without hindering prosurvival Ca2+ signals induced by weak TCR activation.

F. Zhong and M.C. Davis contributed equally to this paper.

Abbreviations used in this paper: InsP3, inositol 1,4,5-trisphosphate; NFAT, nuclear factor of activated T cells; siRNA, small interfering RNA; TCR, T cell receptor.


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