ArticleJournal of immunology research2014
Roles of TLR3 and RIG-I in mediating the inflammatory response in mouse microglia following Japanese encephalitis virus infection.
Article in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 126 citations in OpenAlex.
- SAMSN1 restricts Japanese encephalitis virus replication by recruiting TRIM21 to degrade viral proteins and activate the interferon pathway.Veterinary research · 2026Article
- Protein Posttranslational Modifications in Immunity: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Japanese Encephalitis Virus and Host Innate Immunity: Insights Into TLR Signaling, PRR Crosstalk, and Viral Immune Evasion.Cell biochemistry and function · 2026Review
- STING is a key driver of Japanese encephalitis virus induced inflammatory response.Communications biology · 2026Article
- Z-DNA binding protein 1 mediates necroptotic cell death in primary murine microglia following herpes simplex virus-1 infection.Journal of neurovirology · 2026Article
- Mechanisms and Clinical Significance of Endosomal Toll-Like Receptors in Neurological Diseases.Molecular neurobiology · 2025Review
- Telmisartan, an anti-hypertensive drug, impedes JEV infection, possibly via the AT1/PPARγ axis.Microbiology spectrum · 2025Article
- Interplay between innate immune cells and inflammatory mediators in dengue infection: an evolving therapeutic paradigm.Expert reviews in molecular medicine · 2025Review
- The slow progression of Japanese encephalitis in aged mice is likely associated to B cell recruitment in the brain.Virologica Sinica · 2025Article
- Japanese encephalitis virus NS1 inhibits IFN-β production by interacting with DDX3X.Journal of virology · 2025Article
- Rosmarinic acid-mediated downregulation of RIG-I and p62 in microglia confers resistance to Japanese encephalitis virus-induced inflammation.BMC veterinary research · 2024Article
- Nucleic acid sensing in the central nervous system: Implications for neural circuit development, function, and degeneration.Immunological reviews · 2024Review
- The enhancer RNA, AANCR, regulates APOE expression in astrocytes and microglia.Nucleic acids research · 2024Article
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- Single-cell RNA sequencing reveals the immune features and viral tropism in the central nervous system of mice infected with Japanese encephalitis virus.Journal of neuroinflammation · 2024Article
- Roles in Innate Immunity.Advances in neurobiology · 2024Review
- Porcine promyelocytic leukemia protein isoforms suppress Japanese encephalitis virus replication in PK15 cells.Virology journal · 2023Article
- The RLR intrinsic antiviral system is expressed in neural retina and restricts lentiviral transduction of human Mueller cells.Experimental eye research · 2023Article
- Viral inhibitory potential of hyoscyamine in Japanese encephalitis virus-infected embryonated chicken eggs involving multiple signaling pathways.Archives of virology · 2023Article
- Metabolic response to CNS infection with flaviviruses.Journal of neuroinflammation · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Japanese encephalitis virus (JEV) infection can cause central nervous system disease with irreversible neurological damage in humans and animals. Evidence suggests that overactivation of microglia leads to greatly increased neuronal damage during JEV infection. However, the mechanism by which JEV induces the activation of microglia remains unclear. Toll-like receptor 3 (TLR3) and retinoic acid-inducible gene I (RIG-I) can recognize double-stranded RNA, and their downstream signaling results in production of proinflammatory mediators. In this study, we investigated the roles of TLR3 and RIG-I in the inflammatory response caused by JEV infection in the mouse microglial cell line. JEV infection induced the expression of TLR3 and RIG-I and the activation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38MAPK). Knockdown of TLR3 and RIG-I attenuated activation of ERK, p38MAPK, activator protein 1 (AP-1), and nuclear factor κB (NF-κB). Secretion of TNF-α, IL-6, and CCL-2, which was induced by JEV, was reduced by TLR3 and RIG-I knockdown and inhibitors of phosphorylated ERK and p38MAPK. Furthermore, viral proliferation was increased following knockdown of TLR3 and RIG-I. Our findings suggest that the signaling pathways of TLR3 and RIG-I play important roles in the JEV-induced inflammatory response of microglia.
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