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Cellular & Molecular Immunology 2021年第2期18卷 452-460页

作者： Amir Boufenzer Kevin Carrasco Lucie Jolly Benjamin Brustolin Elisa Di-Pillo Marc Derive sébastien gibot INOTREM Vandœuvre-lès-NancyNancyFrance UMR-s 1116 Défaillance Cardiovasculaire Aigue et ChroniqueVandœuvre-lès-NancyNancyFrance CHRU Nancy Hôpital CentralService de Réanimation MédicaleNancyFrance

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.

关键词： TREM-1 NETs sepsis endothelial cell activation vascular dysfunction LR12

TREM-1 expression during major abdominal surgery: Comment on the Gonzalez-Roldan et al paper

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World Journal of Gastroenterology 2006年第29期12卷 4767-4767页

作者： sebastien gibot service de Réanimation Médicale H(o|^)pital Central and Laboratoire de Physiologie Expérimentale (Groupe Choc)Faculté de MédecineNancyFrance

TO THE EDITOR I read with a great interest the paper by Gonzalez-Roldan et al. The authors reported on the pattern expression of TREM-1 during sepsis and major abdominal surgery as compared to healthy controls and con... 详细信息

关键词：腹部损伤手术治疗临床病理机制

TREM-1 multimerization is essential for its activation on monocytes and neutrophils

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Cellular & Molecular Immunology 2019年第5期16卷 460-472页

作者： Kevin Carrasco Amir Boufenzer Lucie Jolly Helene Le Cordier Guanbo Wang Albert JR Heck Adelheid Cerwenka Emilie Vinolo Alexis Nazabal Alexandre Kriznik Pierre Launay sebastien gibot Marc Derive INOTREM Vandœuvre-les-NancyFrance UMR-s 1116 Defaillance cardiovasculaire aigue et chroniqueVandœuvre-les-NancyFrance UMR7365 Ingénierie Moléculaire et Physiopathologie Articulaire(IMoPA)CNRS-Universitéde LorraineVandœuvre-les-NancyFrance Biomolecular Mass spectrometry and Proteomics Bijvoet Center for Biomolecular Research and Utrecht Institute for Pharmaceutical Sciences and Netherlands Proteomics CenterUtrecht UniversityUtrechtThe Netherlands Innate Immunity German Cancer Research Center(DKFZ)HeidelbergGermany CovalX ZurichSwitzerland service Commun de Biophysique Interactions Moléculaires(sCBIM) FR3209Biopole de l’Universitede LorraineVandœuvre-les-NancyFrance Inatherys Evry CedexFrance

The triggering receptor expressed on myeloid cells-1(TREM-1)is a receptor expressed on innate immune cells.By promoting the amplification of inflammatory signals that are initially triggered by Toll-like receptors(TLRs),TREM-1 has been characterized as a major player in the pathophysiology of acute and chronic inflammatory diseases,such as septic shock,myocardial infarction,atherosclerosis,and inflammatory bowel diseases.However,the molecular events leading to the activation of TREM-1 in innate immune cells remain unknown.Here,we show that TREM-1 is activated by multimerization and that the levels of intracellular Ca 2+release,reactive oxygen species,and cytokine production correlate with the degree of TREM-1 aggregation.TREM-1 activation on primary human monocytes by LPs required a two-step process consisting of upregulation followed by clustering of TREM-1 at the cell surface,in contrast to primary human neutrophils,where LPs induced a rapid cell membrane reorganization of TREM-1,which confirmed that TREM-1 is regulated differently in primary human neutrophils and monocytes.In addition,we show that the ectodomain of TREM-1 is able to homooligomerize in a concentration-dependent manner,which suggests that the clustering of TREM-1 on the membrane promotes its oligomerization.We further show that the adapter protein DAP12 stabilizes TREM-1 surface expression and multimerization.TREM-1 multimerization at the cell surface is also mediated by its endogenous ligand,a conclusion supported by the ability of the TREM-1 inhibitor LR12 to limit TREM-1 multimerization.These results provide evidence for ligand-induced,receptor-mediated dimerization of TREM-1.Collectively,our findings uncover the mechanisms necessary for TREM-1 activation in monocytes and neutrophils.

关键词： TREM-1 multimerization activation monocytes neutrophils

sTREM-1 is a specific biomarker of TREM-1 pathway activation

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Cellular & Molecular Immunology 2021年第8期18卷 2054-2056页

作者： Lucie Jolly Kévin Carrasco Margarita salcedo-Magguilli Jean-Jacques Garaud simon Lambden Tom van der Poll Alexandre Mebazaa Pierre-François Laterre sebastien gibot Amir Boufenzer Marc Derive Inotrem Vandœuvre-lès-NancyFrance Division of Infectious Diseases Amsterdam University Medical CentersUniversity of AmsterdamAmsterdamThe Netherlands Intensive Care Unit Saint Louis-Lariboisière-Fernand Widal University HospitalAssistance Publique Hôpitaux de Parisand Universitéde ParisInserm MASCOTParisFrance Intensive Care Unit UniversitéCatholique de LouvainLouvain-la-NeuveBelgium Intensive Care Unit CHRU de Nancyand Universitéde LorraineNancyFrance

TREM-1(triggering receptor expressed on myeloid cells-1)is a transmembrane receptor expressed by innate immune cells,including endothelial cells and platelets.TREM-1 is a crucial mediator of septic shock that acts by synergizing with Toll-like receptors(TLRs)to amplify the inflammatory responses to pathogens,thus promoting sepsis-induced immune dysregulation and organ dysfunction[1,2,3].

关键词： immune myeloid activation