Regulation of neutrophil apoptosis via death receptors

被引:61
作者
Akgul, C
Edwards, SW
机构
[1] Canakkale Onsekiz Mart Univ, Fac Arts & Sci, Dept Biochem, TR-17100 Canakkale, Turkey
[2] Univ Liverpool, Sch Biol Sci, Liverpool L69 7ZB, Merseyside, England
关键词
neutrophil; apoptosis; death receptor; TNF-alpha; Fas; protein kinase; anti-TNF-alpha;
D O I
10.1007/s00018-003-3110-z
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Human neutrophils constitutively undergo apoptosis, process which is critical for the successful resolution of inflammation by the safe removal of effete cells. A wide variety of agents can modulate neutrophil apoptosis and these act through multiple and complex receptor-signalling pathways. Whilst these pathways can be initiated via distinct cell surface receptors, many downstream intracellular pathways can converge, use common molecules or trigger similar cellular activities, such as activation of caspases and transcription factors. The cell surface receptors, TNFR and Fas both trigger apoptosis in certain cell types, including neutrophils. However, TNF receptors also activate survival mechanisms in human neutrophils. This review summarises current knowledge about the regulation of neutrophil apoptosis via death receptors, the molecular components involved in signalling and potential therapeutic targets that are based on death receptors or their signalling pathways.
引用
收藏
页码:2402 / 2408
页数:7
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