ArticleGlia2009
Theiler's virus infection induces TLR3-dependent upregulation of TLR2 critical for proinflammatory cytokine production.
Article in Glia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 43 citations in OpenAlex.
- Editorial: The role of toll-like receptors and their related signaling pathways in viral infection and inflammation.Frontiers in immunology · 2024Article
- Critical role of TLR activation in viral replication, persistence, and pathogenicity of Theiler's virus.Frontiers in immunology · 2023Review
- Toll-like Receptors in Viral Encephalitis.Viruses · 2021Review
- Excessive Innate Immunity Steers Pathogenic Adaptive Immunity in the Development of Theiler's Virus-Induced Demyelinating Disease.International journal of molecular sciences · 2021Review
- Rapid Expansion of Virus-Specific CD4International journal of molecular sciences · 2020Article
- Endothelin-1 contributes to the development of virus-induced demyelinating disease.Journal of neuroinflammation · 2020Article
- Article
- Facets of Theiler's Murine Encephalomyelitis Virus-Induced Diseases: An Update.International journal of molecular sciences · 2019Review
- Effects of Keratinocyte-Derived Cytokine (CXCL-1) on the Development of Theiler's Virus-Induced Demyelinating Disease.Frontiers in cellular and infection microbiology · 2018Article
- Prostaglandin E2 produced following infection with Theiler's virus promotes the pathogenesis of demyelinating disease.PloS one · 2017Article
- TLR2 and TLR9 modulate enteric nervous system inflammatory responses to lipopolysaccharide.Journal of neuroinflammation · 2016Article
- Transgenic expression of non-structural genes of Theiler's virus suppresses initial viral replication and pathogenesis of demyelination.Journal of neuroinflammation · 2016Article
- Interferon-stimulated genes-essential antiviral effectors implicated in resistance to Theiler's virus-induced demyelinating disease.Journal of neuroinflammation · 2015Article
- The level of viral infection of antigen-presenting cells correlates with the level of development of Theiler's murine encephalomyelitis virus-induced demyelinating disease.Journal of virology · 2015Article
- Interleukin-6 (IL-6) and IL-17 synergistically promote viral persistence by inhibiting cellular apoptosis and cytotoxic T cell function.Journal of virology · 2014Article
- Toll-like receptors in antiviral innate immunity.Journal of molecular biology · 2014Review
- The role of interleukin-6 in the expression of PD-1 and PDL-1 on central nervous system cells following infection with Theiler's murine encephalomyelitis virus.Journal of virology · 2013Article
- The epitope integration site for vaccine antigens determines virus control while maintaining efficacy in an engineered cancer vaccine.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Article
- IL-1 signal affects both protection and pathogenesis of virus-induced chronic CNS demyelinating disease.Journal of neuroinflammation · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Theiler's murine encephalomyelitis virus (TMEV) infection directly induces many proinflammatory genes, including type I interferon (IFN) and a variety of cytokine genes. These virus-induced cytokines are a critical factor in developing TMEV-induced demyelinating disease. We have previously reported that the major activation signal for the cytokine genes is mediated via TLR3. In this study, we describe that TLR2 is upregulated via TLR3 signal and cooperatively participates in the expression of IL-6, IL-1beta, CCL2, and CCL5 genes following TMEV infection. The expression of these genes was significantly impaired in both TLR2-deficient and TLR3-deficient primary astrocytes. However, the induction of type I IFNs was not affected by TLR2 deficiency in the primary cells. TMEV infection led to TLR2-mediated NF-kappaB activation, but not IRF3 or IRF7 activation, critical for type I IFN production. More importantly, TLR3 was required for TMEV-induced early TLR2 upregulation in primary astrocytes leading to the production of TLR2-dependent cytokines such as IL-6. Interestingly, soluble factor(s) produced via TLR2/3-dependent signals appears to be partially associated with the downstream cytokine production. These results indicate that TMEV utilizes TLR3-induced TLR2 to induce inflammatory cytokines, which are critical to the development of immune-mediated demyelinating disease.
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What OpenQuestion holds
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.