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

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 *** 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 ***,the molecular events leading to the activation of TREM-1 in innate immune cells remain ***,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 ***-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 *** 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 *** further show that the adapter protein DAP12 stabilizes TREM-1 surface expression and ***-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 *** results provide evidence for ligand-induced,receptor-mediated dimerization of ***,our findings uncover the mechanisms necessary for TREM-1 activation in monocytes and neutrophils.

关键词： TREM-1 multimerization activation monocytes neutrophils

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