{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Terada Y"],"funding":["BLRD VA","NIBIB NIH HHS","NIAID NIH HHS","NHLBI NIH HHS","NIAMS NIH HHS"],"pagination":["115380"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12756909"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["44(3)"],"pubmed_abstract":["Triggering receptor expressed on myeloid cells 1 (TREM-1) has been shown to amplify inflammatory signals, such as Toll-like receptor signaling, after infection and sterile injury. While previous studies have demonstrated that TREM-1 activation in circulating immune cells promotes injury, the role of TREM-1 signaling in tissue-resident cells in the context of sterile inflammation remains poorly understood. Here, we used a cardiac transplantation model to dissect how Trem1/3 expression on heart-resident cells regulates sterile inflammation. TREM-1 is expressed in heart-resident C-C chemokine receptor 2 (CCR2)<sup>+</sup> macrophages in mice and humans. TREM-1/3 signaling in tissue-resident CCR2<sup>+</sup> macrophages promotes C-C motif chemokine ligand 3 (CCL3) production and is critical fo"],"journal":["Cell reports"],"pubmed_title":["Tissue-resident CCR2&lt;sup&gt;+&lt;/sup&gt; macrophage TREM-1/3 signaling is necessary for monocyte and neutrophil recruitment to injured hearts."],"pmcid":["PMC12756909"],"funding_grant_id":["I01 BX002730","P30 AR073752","R35 HL161185","R01 HL151078","P01 AI116501","R01 HL094601","P41 EB025815","R35 HL145212"],"pubmed_authors":["Nava RG","Gelman AE","Heo GS","Colonna M","Wein AN","Lavine KJ","Kreisel D","Bery AI","Prabhu SD","Terada Y","Li W","Dun H","Koenig AL","Liu Y","Cella M","Luehmann HP","Ritter JH","Liu CR","Owen MC","Frye CC","Amrute JM","Nunna V"],"additional_accession":[]},"is_claimable":false,"name":"Tissue-resident CCR2&lt;sup&gt;+&lt;/sup&gt; macrophage TREM-1/3 signaling is necessary for monocyte and neutrophil recruitment to injured hearts.","description":"Triggering receptor expressed on myeloid cells 1 (TREM-1) has been shown to amplify inflammatory signals, such as Toll-like receptor signaling, after infection and sterile injury. While previous studies have demonstrated that TREM-1 activation in circulating immune cells promotes injury, the role of TREM-1 signaling in tissue-resident cells in the context of sterile inflammation remains poorly understood. Here, we used a cardiac transplantation model to dissect how Trem1/3 expression on heart-resident cells regulates sterile inflammation. TREM-1 is expressed in heart-resident C-C chemokine receptor 2 (CCR2)<sup>+</sup> macrophages in mice and humans. TREM-1/3 signaling in tissue-resident CCR2<sup>+</sup> macrophages promotes C-C motif chemokine ligand 3 (CCL3) production and is critical fo","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-06-09T05:17:14.318Z","creation":"2026-06-09T03:07:44.353Z"},"accession":"S-EPMC12756909","cross_references":{"pubmed":["40042972"],"doi":["10.1016/j.celrep.2025.115380"]}}