ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Conditional ablation of astroglial CCL2 suppresses CNS accumulation of M1 macrophages and preserves axons in mice with MOG peptide EAE.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
73 citing papers in PubMed, 136 citations in OpenAlex.
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026Review
- Antigen-specific adaptive immunity in Parkinson's disease: peripheral priming, brain-border reactivation and parenchymal injury.Journal of neuroinflammation · 2026Review
- Innate Immunity in the Pathogenesis of Selected Autoimmune Neurological Diseases.Journal of clinical medicine · 2025Review
- From diagnosis to treatment: exploring the mechanisms underlying optic neuritis in multiple sclerosis.Journal of translational medicine · 2025Review
- Respiratory infection with influenza A virus delays remyelination and alters oligodendrocyte metabolism.iScience · 2024Article
- CSF1R antagonism results in increased supraspinal infiltration in EAE.Journal of neuroinflammation · 2024Article
- Neuroinflammation, memory, and depression: new approaches to hippocampal neurogenesis.Journal of neuroinflammation · 2023Review
- Peripheral immune system modulates Purkinje cell degeneration in Niemann-Pick disease type C1.Life science alliance · 2023Article
- The impact of phyto- and endo-cannabinoids on central nervous system diseases：A review.Journal of traditional and complementary medicine · 2023Review
- Glial Cells of the Central Nervous System: A Potential Target in Chronic Prostatitis/Chronic Pelvic Pain Syndrome.Pain research & management · 2023Review
- Review
- NADProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Function and therapeutic value of astrocytes in neurological diseases.Nature reviews. Drug discovery · 2022Review
- ASK1 signaling regulates phase-specific glial interactions during neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- 4R-cembranoid protects neuronal cells from oxygen-glucose deprivation by modulating microglial cell activation.Brain research bulletin · 2022Article
- Impact of histone modifier-induced protection against autoimmune encephalomyelitis on multiple sclerosis treatment.Frontiers in neurology · 2022Review
- Cells of the Blood-Brain Barrier: An Overview of the Neurovascular Unit in Health and Disease.Methods in molecular biology (Clifton, N.J.) · 2022Review
- Chemokine-Driven Migration of Pro-Inflammatory CD4Frontiers in immunology · 2022Review
- Astrocytes and Inflammatory T Helper Cells: A Dangerous Liaison in Multiple Sclerosis.Frontiers in immunology · 2022Review
13 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
7 authors at 2 institutions in 1 country.
Funding
Abstract
Current multiple sclerosis (MS) therapies only partially prevent chronically worsening neurological deficits, which are largely attributable to progressive loss of CNS axons. Prior studies of experimental autoimmune encephalomyelitis (EAE) induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG peptide), a model of MS, documented continued axon loss for months after acute CNS inflammatory infiltrates had subsided, and massive astroglial induction of CCL2 (MCP-1), a chemokine for CCR2(+) monocytes. We now report that conditional deletion of astroglial CCL2 significantly decreases CNS accumulation of classically activated (M1) monocyte-derived macrophages and microglial expression of M1 markers during the initial CNS inflammatory phase of MOG peptide EAE, reduces the acute and long-term severity of clinical deficits and slows the progression of spinal cord axon loss. In addition, lack of astroglial-derived CCL2 results in increased accumulation of Th17 cells within the CNS in these mice, but also in greater confinement of CD4(+) lymphocytes to CNS perivascular spaces. These findings suggest that therapies designed to inhibit astroglial CCL2-driven trafficking of monocyte-derived macrophages to the CNS during acute MS exacerbations have the potential to significantly reduce CNS axon loss and slow progression of neurological deficits.
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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.