ArticleScientific reports2015
CD11c(hi) Dendritic Cells Regulate Ly-6C(hi) Monocyte Differentiation to Preserve Immune-privileged CNS in Lethal Neuroinflammation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Balancing functions of regulatory T cells in mosquito-borne viral infections.Emerging microbes & infections · 2024Review
- Role of inflammatory cytokine burst in neuro-invasion of Japanese Encephalitis virus infection: an immunotherapeutic approaches.Journal of neurovirology · 2024Review
- Advances in viral encephalitis: Viral transmission, host immunity, and experimental animal models.Zoological research · 2023Review
- Mice as an Animal Model for Japanese Encephalitis Virus Research: Mouse Susceptibility, Infection Route, and Viral Pathogenesis.Pathogens (Basel, Switzerland) · 2023Review
- Japanese Encephalitis Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- JEV Infection Induces M-MDSC Differentiation Into CD3Frontiers in immunology · 2022Article
- Systemic Immunomodulatory Effects of Combinatorial Treatment of Thalidomide and Dexamethasone on T Cells and Other Immune Cells.Yonsei medical journal · 2021Article
- Japanese Encephalitis Virus Infected Human Monocyte-Derived Dendritic Cells Activate a Transcriptional Network Leading to an Antiviral Inflammatory Response.Frontiers in immunology · 2021Article
- Japanese encephalitis virus and its mechanisms of neuroinvasion.PLoS pathogens · 2020Article
- Recent advances in understanding Japanese encephalitis.F1000Research · 2019Review
- Cryptic etiopathological conditions of equine nervous system with special emphasis on viral diseases.Veterinary world · 2017Review
- Regulation of inflammation in Japanese encephalitis.Journal of neuroinflammation · 2017Review
- Exacerbation of Japanese Encephalitis by CD11cImmune network · 2017Article
- Critical roles of conventional dendritic cells in promoting T cell-dependent hepatitis through regulating natural killer T cells.Clinical and experimental immunology · 2017Article
- Article
- CCR5 ameliorates Japanese encephalitis via dictating the equilibrium of regulatory CD4(+)Foxp3(+) T and IL-17(+)CD4(+) Th17 cells.Journal of neuroinflammation · 2016Article
- IL-33 signaling is essential to attenuate viral-induced encephalitis development by downregulating iNOS expression in the central nervous system.Journal of neuroinflammation · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the roles of dendritic cells (DCs) in adaptive defense have been defined well, the contribution of DCs to T cell-independent innate defense and subsequent neuroimmunopathology in immune-privileged CNS upon infection with neurotropic viruses has not been completely defined. Notably, DC roles in regulating innate CD11b(+)Ly-6C(hi) monocyte functions during neuroinflammation have not yet been addressed. Using selective ablation of CD11c(hi)PDCA-1(int/lo) DCs without alteration in CD11c(int)PDCA-1(hi) plasmacytoid DC number, we found that CD11c(hi) DCs are essential to control neuroinflammation caused by infection with neurotropic Japanese encephalitis virus, through early and increased infiltration of CD11b(+)Ly-6C(hi) monocytes and higher expression of CC chemokines. More interestingly, selective CD11c(hi) DC ablation provided altered differentiation and function of infiltrated CD11b(+)Ly-6C(hi) monocytes in the CNS through Flt3-L and GM-CSF, which was closely associated with severely enhanced neuroinflammation. Furthermore, CD11b(+)Ly-6C(hi) monocytes generated in CD11c(hi) DC-ablated environment had a deleterious rather than protective role during neuroinflammation, and were more quickly recruited into inflamed CNS, depending on CCR2, thereby exacerbating neuroinflammation via enhanced supply of virus from the periphery. Therefore, our data demonstrate that CD11c(hi) DCs provide a critical and unexpected role to preserve the immune-privileged CNS in lethal neuroinflammation via regulating the differentiation, function, and trafficking of CD11b(+)Ly-6C(hi) monocytes.
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