ArticleThe Journal of experimental medicine2015
TREM-2 promotes macrophage survival and lung disease after respiratory viral infection.
Article in The Journal of experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
134 citing papers in PubMed, 207 citations in OpenAlex.
- TREM2 drives monocyte-derived macrophage responses tobioRxiv : the preprint server for biology · 2026Article
- Triggering Receptor Expressed on Myeloid Cells-2 Regulates Innate Lymphoid Cell Levels in Bleomycin-Induced Pulmonary Fibrosis.The Kaohsiung journal of medical sciences · 2026Article
- Temporal upregulation of TREM2 parallel to M2 macrophage marker expression in tuberculosis: implications for macrophage polarization regulation.Frontiers in cellular and infection microbiology · 2026Article
- TREM2 promotes adipogenesis of PDGFR-αFrontiers in endocrinology · 2026Article
- Trem2 activation by renal tubular debris sustains Arg1Frontiers in immunology · 2026Article
- The Role of TREM2 After Stroke: From Mechanisms to Therapeutic Potential.Molecular neurobiology · 2025Review
- TREM2-driven peripheral macrophage regulation in inflammatory diseases: implications extending beyond neurological disorders.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- CRISPR-MI and scRNA-Seq Reveal TREM2's Function in Monocyte Infiltration and Macrophage Apoptosis During Abdominal Aortic Aneurysm Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Clinical Interventions and Inflammatory Signaling Shape the Transcriptional and Cellular Architecture of the Early Postnatal Lung.bioRxiv : the preprint server for biology · 2025Article
- Is TREM2 a Stretch: Implications of TREM2 Along Spinal Cord Circuits in Health, Aging, Injury, and Disease.Cells · 2025Review
- Multimodal profiling reveals tissue-directed signatures of human immune cells altered with age.Nature immunology · 2025Article
- Genetic variation in the activity of a TREM2-p53 signaling axis determines oxygen-induced lung injury.Nature immunology · 2025Article
- The role of immune checkpoint molecules in PRRSV-2-induced immune modulation: insights from comparativeJournal of virology · 2025Article
- Balancing Microglial Density and Activation in Central Nervous System Development and Disease.Current issues in molecular biology · 2025Review
- The late-onset Alzheimer's disease risk factor RHBDF2 is a modifier of microglial TREM2 proteolysis.Life science alliance · 2025Article
- Analysis and interpretation of inflammatory fluid markers in Alzheimer's disease: a roadmap for standardization.Journal of neuroinflammation · 2025Review
- Single-cell transcriptomics of bronchoalveolar lavage during PRRSV infection with different virulence.Nature communications · 2025Article
- TREM2Frontiers in immunology · 2025Review
- Compromised C3b-VSIG4 axis between decidual NK cells and macrophages contributes to recurrent spontaneous abortion.Journal of translational medicine · 2024Article
- The double-edged role and therapeutic potential of TREM2 in atherosclerosis.Biomarker research · 2024Review
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Viral infections and type 2 immune responses are thought to be critical for the development of chronic respiratory disease, but the link between these events needs to be better defined. Here, we study a mouse model in which infection with a mouse parainfluenza virus known as Sendai virus (SeV) leads to long-term activation of innate immune cells that drive IL-13-dependent lung disease. We find that chronic postviral disease (signified by formation of excess airway mucus and accumulation of M2-differentiating lung macrophages) requires macrophage expression of triggering receptor expressed on myeloid cells-2 (TREM-2). Analysis of mechanism shows that viral replication increases lung macrophage levels of intracellular and cell surface TREM-2, and this action prevents macrophage apoptosis that would otherwise occur during the acute illness (5-12 d after inoculation). However, the largest increases in TREM-2 levels are found as the soluble form (sTREM-2) long after clearance of infection (49 d after inoculation). At this time, IL-13 and the adapter protein DAP12 promote TREM-2 cleavage to sTREM-2 that is unexpectedly active in preventing macrophage apoptosis. The results thereby define an unprecedented mechanism for a feed-forward expansion of lung macrophages (with IL-13 production and consequent M2 differentiation) that further explains how acute infection leads to chronic inflammatory disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.