Requirement for caspase-8 in NF-κB activation by antigen receptor

被引：352

作者：

Su, H

Bidère, N

Zheng, LX

Cubre, A

Sakai, K

Dale, J

Salmena, L

Hakem, R

Straus, S

Lenardo, M

机构：

[1] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA

[2] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA

[3] Univ Toronto, Ontario Canc Inst, Toronto, ON M5G 2C1, Canada

来源：

SCIENCE | 2005年 / 307卷 / 5714期

关键词：

D O I：

10.1126/science.1104765

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：

Caspase-8, a proapoptotic protease, has an essential role in lymphocyte activation and protective immunity. We show that caspase-8 deficiency (CED) in humans and mice specifically abolishes activation of the transcription factor nuclear factor kappaB (NF-kappaB) after stimulation through antigen receptors, Fc receptors, or Toll-like receptor 4 in T, B, and natural killer cells. Caspase-8 also causes the up complex of the inhibitor of NF-kappaB kinase (IKK) to associate with the upstream Bcl10-MALT1 (mucosa-associated lymphatic tissue) adapter complex. Recruitment of the IKKalpha,beta complex, its activation, and the nuclear translocation of NF-kappaB require enzyme activity of full-length caspase-8. These findings thus explain the paradoxical association of defective apoptosis and combined immunodeficiency in human CED.

引用

收藏

页码：1465 / 1468

页数：4

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