ArticleImmunology2016
CCL2, but not its receptor, is essential to restrict immune privileged central nervous system-invasion of Japanese encephalitis virus via regulating accumulation of CD11b(+) Ly-6C(hi) monocytes.
Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- Spatial transcriptomics uncovers vasculature-centered cellular interactions driving Japanese encephalitis progression in a mouse model.Nature communications · 2026Article
- Spatial gene expression analysis reveals pathological niches in Japanese encephalitis virus neuroinvasion.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- "Silent messengers of chaos: unveiling the dual threat of immune infiltrates in Japanese encephalitis virus neuroinflammatory storm".Virology journal · 2025Review
- Understanding the pro- & anti-inflammatory cytokine profile in Japanese encephalitis & their implications in survival outcome.The Indian journal of medical research · 2025Article
- Article
- Leukocyte recruitment in flavivirus-induced encephalitis.Frontiers in immunology · 2025Review
- Orchestration of antiviral responses within the infected central nervous system.Cellular & molecular immunology · 2024Review
- Role of inflammatory cytokine burst in neuro-invasion of Japanese Encephalitis virus infection: an immunotherapeutic approaches.Journal of neurovirology · 2024Review
- A Pocket Guide to CCR5-Neurotropic Flavivirus Edition.Viruses · 2023Review
- Mice as an Animal Model for Japanese Encephalitis Virus Research: Mouse Susceptibility, Infection Route, and Viral Pathogenesis.Pathogens (Basel, Switzerland) · 2023Review
- Exaggerated levels of some specific TLRs, cytokines and chemokines in Japanese encephalitis infected BV2 and neuro 2A cell lines associated with worst outcome.Virology journal · 2023Article
- JEV Infection Induces M-MDSC Differentiation Into CD3Frontiers in immunology · 2022Article
- The increased intrathecal expression of the monocyte-attracting chemokines CCL7 and CXCL12 in tick-borne encephalitis.Journal of neurovirology · 2021Article
- Peripheral Injection of Tim-3 Antibody Attenuates VSV Encephalitis by Enhancing MHC-I Presentation.Frontiers in immunology · 2021Article
- Synthetic Host Defense Peptides Inhibit Venezuelan Equine Encephalitis Virus Replication and the Associated Inflammatory Response.Scientific reports · 2020Article
- CCR2 Inhibition Reduces Neurotoxic Microglia Activation Phenotype After Japanese Encephalitis Viral Infection.Frontiers in cellular neuroscience · 2020Article
- PD1Virologica Sinica · 2019Article
- Neuroinflammation During RNA Viral Infections.Annual review of immunology · 2019Review
- Japanese encephalitis - the prospects for new treatments.Nature reviews. Neurology · 2018Review
- Cutting Edge: CCR2 Is Not Required for Ly6CJournal of immunology (Baltimore, Md. : 1950) · 2018Article
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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
Japanese encephalitis virus (JEV) is a re-emerging zoonotic flavivirus that poses an increasing threat to global health and welfare due to rapid changes in climate and demography. Although the CCR2-CCL2 axis plays an important role in trafficking CD11b(+) Ly-6C(hi) monocytes to regulate immunopathological diseases, little is known about their role in monocyte trafficking during viral encephalitis caused by JEV infection. Here, we explored the role of CCR2 and its ligand CCL2 in JE caused by JEV infection using CCR2- and CCL2-ablated murine models. Somewhat surprisingly, the ablation of CCR2 and CCL2 resulted in starkly contrasting susceptibility to JE. CCR2 ablation induced enhanced resistance to JE, whereas CCL2 ablation highly increased susceptibility to JE. This contrasting regulation of JE progression by CCR2 and CCL2 was coupled to central nervous system (CNS) infiltration of Ly-6C(hi) monocytes and Ly-6G(hi) granulocytes. There was also enhanced expression of CC and CXC chemokines in the CNS of CCL2-ablated mice, which appeared to induce CNS infiltration of these cell populations. However, our data revealed that contrasting regulation of JE in CCR2- and CCL2-ablated mice was unlikely to be mediated by innate natural killer and adaptive T-cell responses. Furthermore, CCL2 produced by haematopoietic stem cell-derived leucocytes played a dominant role in CNS accumulation of Ly-6C(hi) monocytes in infected bone marrow chimeric models, thereby exacerbating JE progression. Collectively, our data indicate that CCL2 plays an essential role in conferring protection against JE caused by JEV infection. In addition, blockage of CCR2, but not CCL2, will aid in the development of strategies for prophylactics and therapeutics of JE.
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