Antigen-mediated T cell expansion regulated by parallel pathways of death

被引：115

作者：

Ch'en, Irene L. ^{[1
,2
]}

Beisner, Daniel R. ^{[1
,2
]}

Degterev, Alexei ^{[4
]}

Lynch, Candace ^{[3
]}

Yuan, Junying ^{[5
]}

Hoffmann, Alexander ^{[3
]}

Hedrick, Stephen M. ^{[1
,2
]}

机构：

[1] Univ Calif San Diego, Div Biol Sci, La Jolla, CA 92093 USA

[2] Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA

[3] Univ Calif San Diego, Dept Chem & Biochem, La Jolla, CA 92093 USA

[4] Tufts Univ, Sch Med, Dept Biochem, Boston, MA 02111 USA

[5] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2008年 / 105卷 / 45期

基金：

美国国家卫生研究院;

关键词：

apoptosis; necrosis; NF kappa B; Ripk1; autophagy;

D O I：

10.1073/pnas.0808043105

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

T cells enigmatically require caspase-8, an inducer of apoptosis, for antigen-driven expansion and effective antiviral responses, and yet the pathways responsible for this effect have been elusive. A defect in caspase-8 expression does not affect progression through the cell cycle but causes an abnormally high rate of cell death that is distinct from apoptosis and does not involve a loss of NF kappa B activation. Instead, antigen or mitogen activated Casp8-deficient T cells exhibit an alternative type of cell death similar to programmed necrosis that depends on receptor interacting protein (Ripk1). The selective genetic ablation of caspase-8, NF kappa B, and Ripk1, reveals two forms of cell death that can regulate virus-specific T cell expansion.

引用

页码：17463 / 17468

页数：6