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The proapoptotic factors Bax and Bak regulate T Cell proliferation through control of endoplasmic reticulum Ca(2+) homeostasis.

Abstract：

:The Bcl-2-associated X protein (Bax) and Bcl-2-antagonist/killer (Bak) are essential regulators of lymphocyte apoptosis, but whether they play a role in viable T cell function remains unclear. Here, we report that T cells lacking both Bax and Bak display defects in antigen-specific proliferation because of Ca(2+)-signaling defects. Bax(-/-), Bak(-/-) T cells displayed defective T cell receptor (TCR)- and inositol-1,4,5-trisphosphate (IP(3))-dependent Ca(2+) mobilization because of altered endoplasmic reticulum (ER) Ca(2+) regulation that was reversed by Bax's reintroduction. The ability of TCR-dependent Ca(2+) signals to stimulate mitochondrial NADH production in excess of that utilized for ATP synthesis was dependent on Bax and Bak. Blunting of Ca(2+)-induced mitochondrial NADH elevation in the absence of Bax and Bak resulted in decreased reactive-oxygen-species production, which was required for T cell proliferation. Together, the data establish that Bax and Bak play an essential role in the control of T cell proliferation by modulating ER Ca(2+) release.

journal_name

Immunity

journal_title

Immunity

authors

Jones RG,Bui T,White C,Madesh M,Krawczyk CM,Lindsten T,Hawkins BJ,Kubek S,Frauwirth KA,Wang YL,Conway SJ,Roderick HL,Bootman MD,Shen H,Foskett JK,Thompson CB

doi

10.1016/j.immuni.2007.05.023

subject

Has Abstract

pub_date

2007-08-01 00:00:00

pages

268-80

issue

2

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(07)00363-9

journal_volume

27

pub_type

杂志文章

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