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		题名	作者	年代	出处	被引量
	1	Potentiation of NETs release is novel characteristic of TREM-1 activation and the pharmacological inhibition of TREM-1 could prevent from the deleterious consequences of NETs release in sepsis显示文摘During sepsis,neutrophil activation induces endothelial cell(EC)dysfunction partly through neutrophil extracellular trap(NET)release.The triggering receptor expressed on myeloid cell-1(TREM-1)is an orphan immune receptor that amplifies the inflammatory response mediated by Toll-like receptor-4(TLR4)engagement.Although the key role of TLR4 signaling in NETosis is known,the role of TREM-1 in this process has not yet been investigated.Here,we report that TREM-1 potentiates NET release by human and murine neutrophils and is a component of the NET structure.In contrast,pharmacologic inhibition or genetic ablation of TREM-1 decreased NETosis in vitro and during experimental septic shock in vivo.Moreover,isolated NETs were able to activate ECs and impair vascular reactivity,and these deleterious effects were dampened by TREM-1 inhibition.TREM-1 may,therefore,constitute a new therapeutic target to prevent NETosis and associated endothelial dysfunction.	Amir Boufenzer Kevin Carrasco Lucie Jolly Benjamin Brustolin Elisa Di-Pillo Marc Derive Sébastien Gibot	2021	Cellular & Molecular Immunology2021，18，2：	9

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