How Neutrophils Meet Their End

被引：106

作者：

Lawrence, Shelley M. ^{[1
,2
]}

Corriden, Ross ^{[2
,3
]}

Nizet, Victor ^{[2
,4
]}

机构：

[1] Univ Calif San Diego, Dept Pediat, Coll Med, Div Neonatal Perinatal Med, San Diego, CA 92103 USA

[2] Univ Calif San Diego, Dept Pediat, Coll Med, Div Host Microbe Syst & Therapeut, San Diego, CA 92103 USA

[3] Univ Calif San Diego, Dept Pharmacol, San Diego, CA 92103 USA

[4] Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, San Diego, CA 92103 USA

来源：

TRENDS IN IMMUNOLOGY | 2020年 / 41卷 / 06期

关键词：

BONE-MARROW; STAPHYLOCOCCUS-AUREUS; APOPTOTIC NEUTROPHILS; PROMOTES AUTOPHAGY; CELL-DEATH; PHAGOCYTOSIS; INFLAMMATION; NECROPTOSIS; INHIBITION; PROTEINS;

D O I：

10.1016/j.it.2020.03.008

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Neutrophil death can transpire via diverse pathways and is regulated by interactions with commensal and pathogenic microorganisms, environmental exposures, and cell age. At steady state, neutrophil turnover and replenishment are continually maintained via a delicate balance between host-mediated responses and microbial forces. Disruptions in this equilibrium directly impact neutrophil numbers in circulation, cell trafficking, antimicrobial defenses, and host wellbeing. How neutrophils meet their end is physiologically important and can result in different immunologic consequences. Whereas nonlytic forms of neutrophil death typically elicit anti-inflammatory responses and promote healing, pathways ending with cell membrane rupture may incite deleterious proinflammatory responses, which can exacerbate local tissue injury, lead to chronic inflammation, or precipitate autoimmunity. This review seeks to provide a contemporary analysis of mechanisms of neutrophil death.

引用

页码：531 / 544

页数：14

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