Modulation of immune signalling by inhibitors of apoptosis

被引:125
作者
Beug, Shawn T. [1 ]
Cheung, Herman H. [1 ,4 ]
LaCasse, Eric C. [1 ]
Korneluk, Robert G. [1 ,2 ,3 ]
机构
[1] Childrens Hosp Eastern Ontario, Res Inst, Apoptosis Res Ctr, Ottawa, ON K1H 8L1, Canada
[2] Univ Ottawa, Dept Cellular & Mol Med, Ottawa, ON K1H 8M5, Canada
[3] Univ Ottawa, Dept Biochem Microbiol & Immunol, Ottawa, ON K1H 8M5, Canada
[4] Ontario Inst Canc Res, MaRS Ctr, Toronto, ON M5G 0A3, Canada
基金
加拿大健康研究院;
关键词
NF-KAPPA-B; X-LINKED INHIBITOR; IAP ANTAGONISTS; INFLAMMASOME ACTIVATION; CELLULAR INHIBITORS; UBIQUITIN-LIGASE; XIAP DEFICIENCY; FUSION PROTEIN; CIAP1; SURVIVIN;
D O I
10.1016/j.it.2012.06.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The inhibitor of apoptosis (IAP) genes are critical regulators of multiple pathways that control cell death, proliferation, and differentiation. Several members of the IAP family regulate innate and adaptive immunity through modulation of signal transduction pathways, cytokine production, and cell survival. The regulation of immunity by the IAPs is primarily mediated through the ubiquitin ligase function of cellular IAP (cIAP)1, cIAP2, and X-linked IAP (XIAP), the targets of which impact nuclear factor (NF)-kappa B and mitogen-activated protein kinase (MAPK) signalling pathways. In addition, neuronal apoptosis inhibitory protein (NAIP), cIAP1, and cIAP2 modulate innate immune responses through control of the inflammasome complex. This review examines the role of mammalian IAPs in regulating immunity and describes the implications of a new class of pan-IAP antagonists for the treatment of immune disorders.
引用
收藏
页码:535 / 545
页数:11
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