ArticleJournal of neuroinflammation2019
CSF1R antagonism limits local restimulation of antiviral CD8
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 175 citations in OpenAlex.
- The Key Drivers of Brain Injury by Systemic Inflammatory Responses after Sepsis: Microglia and Neuroinflammation.Molecular neurobiology · 2023Pooled it
- Macrophage-glia interactions regulate immune damage to enteric neurons during West Nile virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Role for NF-κB in herpes encephalitis pathology in mice genocopying an inborn error of IRF3-IFN immunity.The Journal of experimental medicine · 2026Article
- The cell-mediated adaptive immune response to herpes simplex virus type 1 encephalitis: mechanisms and clinical implications.Frontiers in immunology · 2026Review
- Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025Review
- MAVS signaling of long-lived brain-resident myeloid cells is needed during viral encephalitis to adjust the transcriptome of CNS infiltrating CD8Journal of neuroinflammation · 2025Article
- Temporally resolved single-cell RNA sequencing reveals protective and pathological responses during herpes simplex virus CNS infection.Journal of neuroinflammation · 2025Article
- Long-term reprogramming of primed microglia after moderate inhibition of CSF1R signaling.Glia · 2025Article
- Dual immune modulation of microglia in viral encephalitis: current understanding and future perspectives.Frontiers in molecular biosciences · 2025Review
- MAVS signaling shapes microglia responses to neurotropic virus infection.Journal of neuroinflammation · 2024Article
- Tissue niche influences immune and metabolic profiles to Staphylococcus aureus biofilm infection.Nature communications · 2024Article
- Orchestration of antiviral responses within the infected central nervous system.Cellular & molecular immunology · 2024Review
- Age-dependent Powassan virus lethality is linked to glial cell activation and divergent neuroinflammatory cytokine responses in a murine model.Journal of virology · 2024Article
- Cystatin F attenuates neuroinflammation and demyelination following murine coronavirus infection of the central nervous system.Journal of neuroinflammation · 2024Article
- CSF1R antagonism results in increased supraspinal infiltration in EAE.Journal of neuroinflammation · 2024Article
- Preclinical translational platform of neuroinflammatory disease biology relevant to neurodegenerative disease.Journal of neuroinflammation · 2024Article
- Antigen non-specific CD8bioRxiv : the preprint server for biology · 2024Article
- Measuring Antibody-Mediated Tau Fibril Uptake in Microglia by Flow Cytometry.Methods in molecular biology (Clifton, N.J.) · 2024Article
- The Impact of Innate Components on Viral Pathogenesis in the Neurotropic Coronavirus Encephalomyelitis Mouse Model.Viruses · 2023Review
- Low-dose PLX5622 treatment prevents neuroinflammatory and neurocognitive sequelae after sepsis.Journal of neuroinflammation · 2023Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMicroglia are resident macrophages of the central nervous system (CNS) locally maintained through colony-stimulating factor 1 receptor (CSF1R) signaling. Microglial depletion via CSF1R inactivation improves cognition in mouse models of neuroinflammation, but limits virologic control in the CNS of mouse models of neurotropic infections by unknown mechanisms. We hypothesize that CSF1R plays a critical role in myeloid cell responses that restrict viral replication and locally restimulate recruited antiviral T cells within the CNS.
methodsThe impact of CSF1R signaling during West Nile virus infection was assessed in vivo using a mouse model of neurotropic infection. Pharmacological inactivation of CSF1R was achieved using PLX5622 prior to infection with virulent or attenuated strains of West Nile virus (WNV), an emerging neuropathogen. The subsequent effect of CSF1R antagonism on virologic control was assessed by measuring mortality and viral titers in the CNS and peripheral organs. Immune responses were assessed by flow cytometric-based phenotypic analyses of both peripheral and CNS immune cells.
resultsMice treated with CSF1R antagonist prior to infection exhibited higher susceptibility to lethal WNV infection and lack of virologic control in both the CNS and periphery. CSFR1 antagonism reduced B7 co-stimulatory signals on peripheral and CNS antigen-presenting cells (APCs) by depleting CNS cellular sources, which limited local reactivation of CNS-infiltrating virus-specific T cells and reduced viral clearance.
conclusionsOur results demonstrate the impact of CSF1R antagonism on APC activation in the CNS and periphery and the importance of microglia in orchestrating the CNS immune response following neurotropic viral infection. These data will be an important consideration when assessing the benefit of CSF1R antagonism, which has been investigated as a therapeutic for neurodegenerative conditions, in which neuroinflammation is a contributing factor.
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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.