ArticlePLoS pathogens2020
TREM2 suppresses the proinflammatory response to facilitate PRRSV infection via PI3K/NF-κB signaling.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 92 citations in OpenAlex.
- Article
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- Labile iron starvation in embryonic Kupffer cells aggravates MASH via mitochondrial failure and macrophage dysfunction.Cell death & disease · 2026Article
- TREM2 drives monocyte-derived macrophage responses tobioRxiv : the preprint server for biology · 2026Article
- Cannabis use by people with HIV is associated with an anti-inflammatory immunometabolic phenotype in monocyte-derived macrophages.Journal of neuroinflammation · 2026Article
- Small-molecule PS10 inhibits PRRSV replication by targeting HSP90 and multiple viral non-structural proteins.Journal of virology · 2026Article
- Sex Differences in Metabolite-Immune Circuits of Neuroinflammation.Immunological reviews · 2026Review
- CD163 at the crossroads: a viral-exploited immunomodulator.Virology journal · 2026Review
- The biological functions of PRRSV nonstructural protein NSP2 in viral infection and replication and its role in host regulatory mechanisms.Frontiers in veterinary science · 2026Review
- 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
- Proanthocyanidins carbon dots inhibit PRRSV infection by activating Nrf2/ARE to regulate oxidative stress and NLRP3 inflammasome-mediated pyroptosis.Veterinary research · 2025Article
- The role of immune checkpoint molecules in PRRSV-2-induced immune modulation: insights from comparativeJournal of virology · 2025Article
- Strategies and scheming: the war between PRRSV and host cells.Virology journal · 2025Review
- Porcine reproductive and respiratory syndrome virus nsp5 inhibits the activation of the Nrf2/HO-1 pathway by targeting p62 to antagonize its antiviral activity.Journal of virology · 2025Article
- Article
- Single cell transcriptomic analysis reveals tumor immune infiltration by macrophage cells gene signature in lung adenocarcinoma.Discover oncology · 2025Article
- Single-cell transcriptomics of bronchoalveolar lavage during PRRSV infection with different virulence.Nature communications · 2025Article
- Newcastle disease virus induces clathrin-mediated endocytosis to establish infection through the activation of PI3K/AKT signaling pathway by VEGFR2.Journal of virology · 2024Article
- Article
- Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triggering receptor expressed on myeloid cells 2 (TREM2) serves as an anti-inflammatory receptor, negatively regulating the innate immune response. TREM2 is mainly expressed on dendritic cells and macrophages, the target cells of porcine reproductive and respiratory syndrome virus (PRRSV). Thus, we investigated the potential role of TREM2 in PRRSV infection in porcine alveolar macrophages (PAMs). We found that there was an increased expression of TREM2 upon PRRSV infection in vitro. TREM2 silencing restrained the replication of PRRSV, whereas TREM2 overexpression facilitated viral replication. The cytoplasmic tail domain of TREM2 interacted with PRRSV Nsp2 to promote infection. TREM2 downregulation led to early activation of PI3K/NF-κB signaling, thus reinforcing the expression of proinflammatory cytokines and type I interferons. Due to the enhanced cytokine expression, a disintegrin and metalloproteinase 17 was activated to promote the cleavage of membrane CD163, which resulted in suppression of infection. Furthermore, exogenous soluble TREM2 (sTREM2)-mediated inhibition of PRRSV attachment might be attributed to its competitive binding to viral envelope proteins. In pigs, following PRRSV challenge in vivo, the expression of TREM2 in lungs and lymph nodes as well as the production of sTREM2 were significantly increased. These novel findings indicate that TREM2 plays a role in regulating PRRSV replication via the inflammatory response. Therefore, our work describes a novel antiviral mechanism against PRRSV infection and suggests that targeting TREM2 could be a new approach in the control of the PRRSV infection.
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