ArticleFrontiers in cellular and infection microbiology2018
Effects of Keratinocyte-Derived Cytokine (CXCL-1) on the Development of Theiler's Virus-Induced Demyelinating Disease.
Article in Frontiers in cellular and infection microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Article
- Combined Gamma-Rays and Carbon-12 Nuclei Irradiation Modulates Brain Chemokine and Cytokine Production and Improves Spatial Learning in Tau P301S, but not 5xFAD Mouse Line.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2023Article
- IFNAR signaling of neuroectodermal cells is essential for the survival of C57BL/6 mice infected with Theiler's murine encephalomyelitis virus.Journal of neuroinflammation · 2023Article
- Attenuated strain of CVB3 with a mutation in the CAR-interacting region protects against both myocarditis and pancreatitis.Scientific reports · 2021Article
- Excessive Innate Immunity Steers Pathogenic Adaptive Immunity in the Development of Theiler's Virus-Induced Demyelinating Disease.International journal of molecular sciences · 2021Review
- Endothelin-1 contributes to the development of virus-induced demyelinating disease.Journal of neuroinflammation · 2020Article
- Facets of Theiler's Murine Encephalomyelitis Virus-Induced Diseases: An Update.International journal of molecular sciences · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
CXCL-1, also called keratinocyte-derived cytokine (KC), is a predominant chemokine produced in glial cells upon infection with Theiler's murine encephalomyelitis virus (TMEV). In this study, we assessed the role of KC in the development of TMEV-induced demyelinating disease by utilizing polyclonal anti-KC antibodies as well as KC-expressing recombinant TMEV. Our results indicate that the level of KC produced after infection with TMEV or stimulation with various TLRs is significantly higher in various cells from susceptible SJL mice compared to those in cells from resistant B6 mice. SJL mice treated with rabbit anti-KC antibodies displayed accelerated development of TMEV-induced demyelinating disease, elevated viral loads in the CNS and decreased antiviral T cell responses. In addition, infection of susceptible SJL mice with recombinant KC-TMEV produced biologically active KC, which resulted in the accelerated pathogenesis of demyelinating disease and elevated T cell responses to viral antigens compared to mice infected with control recombinant HEL-TMEV. These results strongly suggest that both the lack of KC during TMEV infection and the excessive presence of the chemokine promote the pathogenesis of demyelinating disease. Therefore, a balance in the level of KC during TMEV infection appears to be critically important in controlling the pathogenesis of demyelinating disease.
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