中性粒细胞胞外陷阱
旁观者效应
生物
效应器
细胞生物学
炎症
免疫学
先天免疫系统
免疫系统
微生物学
作者
Valentina Poli,Ivan Zanoni
标识
DOI:10.1016/j.tim.2022.10.002
摘要
Abstract
Neutrophil extracellular traps (NETs) evolved to protect the host against microbial infections and are formed by a web-like structure of DNA that is decorated with antimicrobial effectors. Due to their potent inflammatory functions, NETs also cause tissue damage and can favor and/or aggravate inflammatory diseases. This multipronged activity of NETs requires that the induction, release, and degradation of NETs are tightly regulated. Here we describe the key pathways that are intrinsic to neutrophils and regulate NETosis, and we review the most recent findings on how neutrophil extrinsic factors participate in the formation of NETs. In particular, we emphasize how bystander cells contribute to modifying the capacity of neutrophils to undergo NETosis. Finally, we discuss how these neutrophil extrinsic processes can be harnessed to protect the host against the excessive inflammation elicited by uncontrolled NET release.
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