ArticlePloS one2013
Attenuated inflammatory response in triggering receptor expressed on myeloid cells 2 (TREM2) knock-out mice following stroke.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 128 citations in OpenAlex.
- Trem2 exacerbates ischemic brain injury through Gpnmb in a photothrombotic stroke model.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Interplay between Peripheral and Central Nervous System Myeloid Cells during Aging: Impact for Lade-Life Depression and Alzheimer's Disease.Neuroimmunomodulation · 2026Review
- Mechanisms of Innate Immune Modulation by High-Fat Diet: Implications for Obesity and Asthma.Current allergy and asthma reports · 2025Review
- Models and mechanisms of post-stroke dementia and cognitive impairment.Frontiers in stroke · 2025Article
- TREM2Frontiers in immunology · 2025Review
- Soluble Triggering Receptors Expressed on Myeloid Cells (sTREM) in Acute Ischemic Stroke: A Potential Pathway of sTREM-1 and sTREM-2 Associated with Disease Severity.International journal of molecular sciences · 2024Article
- TREM2 Deficiency Aggravates NLRP3 Inflammasome Activation and Pyroptosis in MPTP-Induced Parkinson's Disease Mice and LPS-Induced BV2 Cells.Molecular neurobiology · 2024Article
- Arresting the bad seed: HDAC3 regulates proliferation of different microglia after ischemic stroke.Science advances · 2024Article
- TREM2-IGF1 Mediated Glucometabolic Enhancement Underlies Microglial Neuroprotective Properties During Ischemic Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Study on pyroptosis-related genes Casp8, Gsdmd and Trem2 in mice with cerebral infarction.PeerJ · 2024Article
- Research on the innate immune response in transgenic mice following ischemic stroke.Frontiers in aging neuroscience · 2024Review
- Function and mechanism of TREM2 in bacterial infection.PLoS pathogens · 2024Review
- Phagocytic microglia and macrophages in brain injury and repair.CNS neuroscience & therapeutics · 2022Review
- AD-16 Protects Against Hypoxic-Ischemic Brain Injury by Inhibiting Neuroinflammation.Neuroscience bulletin · 2022Article
- Soluble TREM2 is associated with death and cardiovascular events after acute ischemic stroke: an observational study from CATIS.Journal of neuroinflammation · 2022Observational
- Triggering receptor expressed on myeloid cells-2 promotes survival of cardiomyocytes after myocardial ischemic injury through PI3K/AKT pathway.Cardiovascular diagnosis and therapy · 2022Article
- Maprotiline ameliorates isoflurane-induced microglial activation via regulating triggering receptor expressed in myeloid cells 2 (TREM2).Bioengineered · 2021Article
- TDP-43 and Inflammation: Implications for Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.International journal of molecular sciences · 2021Review
- Microglial Responses to Brain Injury and Disease: Functional Diversity and New Opportunities.Translational stroke research · 2021Review
- TREM2 alters the phagocytic, apoptotic and inflammatory response to AβMolecular immunology · 2021Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriggering receptor expressed on myeloid cells-2 (TREM2) is a microglial surface receptor involved in phagocytosis. Clearance of apoptotic debris after stroke represents an important mechanism to re-attain tissue homeostasis and thereby ensure functional recovery. The role of TREM2 following stroke is currently unclear. METHODS AND
resultsAs an experimental stroke model, the middle cerebral artery of mice was occluded for 30 minutes with a range of reperfusion times (duration of reperfusion: 6 h/12 h/24 h/2 d/7 d/28 d). Quantitative PCR (qPCR) revealed a greatly increased transcription of TREM2 after stroke. We subsequently analyzed the expression of pro-inflammatory cytokines, chemokines and their receptors in TREM2-knockout (TREM2-KO) mice via qPCR. Microglial activation (CD68, Iba1) and CD3-positive T-cell invasion were analyzed via qPCR and immunohistochemistry. Functional consequences of TREM2 knockout were assessed by infarct volumetry. The acute inflammatory response (12 h reperfusion) was very similar between TREM2-KO mice and their littermate controls. However, in the sub-acute phase (7 d reperfusion) following stroke, TREM2-KO mice showed a decreased transcription of pro-inflammatory cytokines TNFα, IL-1α and IL-1β, associated with a reduced microglial activity (CD68, Iba1). Furthermore, TREM2-KO mice showed a reduced transcription of chemokines CCL2 (MCP1), CCL3 (MIP1α) and the chemokine receptor CX3CR1, followed by a diminished invasion of CD3-positive T-cells. No effect on the lesion size was observed.
conclusionsAlthough we initially expected an exaggerated pro-inflammatory response following ablation of TREM2, our data support a contradictory scenario that the sub-acute inflammatory reaction after stroke is attenuated in TREM2-KO mice. We therefore conclude that TREM2 appears to sustain a distinct inflammatory response after stroke.
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