多形核中性粒细胞（PMN）代表着对侵入病原体的最早防御线，也是循环中最丰富的白细胞。一般被描述为促炎性细胞，最新的数据表明PMN也具有免疫调节能力。在对特定刺激的反应中，被激活的PMN会释放中性粒细胞胞外陷阱（NET），这是由DNA和相关蛋白组成的结构。尽管最初被描述为一种先天免疫机制来对抗细菌感染，但NET形成（或更确切地说是NET过剩和NET清除能力受损）可能是有害的。实际上，NET已被认为与几种炎症性和自身免疫性疾病的发展有关，如类风湿性关节炎或系统性红斑狼疮，以及纤维化或癌症。它们被建议作为（新）自身抗原来源或调节蛋白质，如蛋白酶，或作为物理屏障。已经描述了不同的NET形成机制，取决于刺激物，可能导致PMN死亡或不死。有趣的是，NET既可能具有促炎性作用，也可能具有抗炎性作用，这可能在很大程度上取决于触发NET形成的机制和刺激物。在本综述中，我们将描述NET的促炎和抗炎活性，尤其是NET如何调节免疫反应。© 作者（或其雇主）2023年。在CC BY-NC许可下再使用。不得进行商业再利用。BMJ出版。

Polymorphonuclear neutrophils (PMN) represent one of the first lines of defence against invading pathogens and are the most abundant leucocytes in the circulation. Generally described as pro-inflammatory cells, recent data suggest that PMN also have immunomodulatory capacities. In response to certain stimuli, activated PMN expel neutrophil extracellular traps (NET), structures made of DNA and associated proteins. Although originally described as an innate immune mechanism fighting bacterial infection, NET formation (or probably rather an excess of NET together with impaired clearance of NET) may be deleterious. Indeed, NET have been implicated in the development of several inflammatory and autoimmune diseases as rheumatoid arthritis or systemic lupus erythematosus, as well as fibrosis or cancer. They have been suggested as a source of (neo)autoantigens or regulatory proteins like proteases or to act as a physical barrier. Different mechanisms of NET formation have been described, leading to PMN death or not, depending on the stimulus. Interestingly, NET may be both pro-inflammatory and anti-inflammatory and this probably partly depends on the mechanism, and thus the stimuli, triggering NET formation. Within this review, we will describe the pro-inflammatory and anti-inflammatory activities of NET and especially how NET may modulate immune responses.© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.