ArticleJournal of neuroinflammation2025
A central role for CCR2 in monocyte recruitment and blood-brain barrier disruption during Usutu virus encephalitis.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular insights into glial neuroimmune cross reactivity with CNS antigens and its role in neuroinflammation.Inflammopharmacology · 2026Pooled it
- Article
- Multistage nanomedicine engineering to overcome sequential barriers to glioblastoma treatment: a review.Journal of nanobiotechnology · 2026Review
- The spleen-brain axis in Alzheimer's disease and related dementias: Integrating immune and metabolic regulation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Article
- Severe Usutu Virus Encephalitis Treated With Corticosteroids: A Case Report.Case reports in infectious diseases · 2026Article
- Article
- CD8 T cell dynamics and immune cell trafficking in ZIKV infection: implications for neuroinflammation and therapy.Virology journal · 2025Review
- Treatment Resistant Persister Cells Exploit Macrophage Lipid Metabolism to Sustain Glioblastoma Growth.bioRxiv : the preprint server for biology · 2025Article
- Leukocyte recruitment in flavivirus-induced encephalitis.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Usutu virus (USUV) is an emerging neurotropic flavivirus capable of causing encephalitis in humans. Here, our main goal was to characterize the innate immune response in the brain during USUV encephalitis and to identify strategies to control disease severity. Using an immunocompetent mouse model of USUV encephalitis, we showed that microglia activation, blood-brain barrier (BBB) disruption and inflammatory monocyte recruitment are hallmarks of disease 6 days post infection. Activated microglia were in close association to USUV-infected cells, concomitantly with elevated levels of IL-6, IFN-γ, CCL2, CCL5, CXCL10 and CXCL1 in the brain. Monocyte recruitment was CCR2-dependent and driven by IFN-γ and CCL2 production beneath the brain vasculature. Moreover, CCR2 deficiency inhibited microglia activation and BBB disruption, showing the central role of CCR2 in USUV encephalitis. Accordingly, treatment with dexamethasone prevented pro-inflammatory mediator production and reduced leukocyte recruitment significantly, restraining encephalitis severity. Concluding, USUV encephalitis is driven by CCR2-mediated monocyte recruitment and BBB disruption, and blocked therapeutically by glucocorticoids.
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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.