ArticleJournal of neuroimmunology2014
Astrocyte CCL2 sustains immune cell infiltration in chronic experimental autoimmune encephalomyelitis.
Article in Journal of neuroimmunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
111 citing papers in PubMed, 167 citations in OpenAlex.
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Role of voltage-dependent anion channel 1 in neurodegeneration: Mechanisms, implications, and therapeutic potential.Neural regeneration research · 2026Article
- Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026Review
- ΔJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Innate immune signaling and functions in astrocytes.Nature immunology · 2026Review
- Glial cells in chronic inflammation: diversity, dysfunction and therapeutic targeting.Nature reviews. Immunology · 2026Review
- Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes.International immunology · 2026Article
- Simulated wildfire smoke particulate matter elicits STING-dependent astrocyte-mediated inflammatory signaling and neurotoxicity.Neurotoxicology · 2026Article
- Astrocyte Functional Heterogeneity in Multiple Sclerosis.Journal of clinical neurology (Seoul, Korea) · 2026Review
- Astrocyte Regulation of Spinal Circuit Function.Journal of neurochemistry · 2026Review
- APOE genotype differentially modulates prion pathology in a mouse model.Acta neuropathologica communications · 2026Article
- Glial Cells as Key Mediators in the Pathophysiology of Neurodegenerative Diseases.International journal of molecular sciences · 2026Review
- Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026Review
- Electroacupuncture alleviates blood-brain barrier disruption and neuroinflammation via astrocytic MC4R in a mouse model of multiple sclerosis.Journal of neuroinflammation · 2025Article
- APOE Genotype Differentially Modulates Prion Pathology in a Mouse Model.Research square · 2025Article
- Innate Immunity in the Pathogenesis of Selected Autoimmune Neurological Diseases.Journal of clinical medicine · 2025Review
- Review
- Mapping Molecular Pathways of Multiple Sclerosis: A Gene Prioritization and Network Analysis of White Matter Pathology Transcriptomics.Annals of neurology · 2025Article
- Role of Extracellular Vesicles in the Pathogenesis of Brain Metastasis.Journal of extracellular biology · 2025Review
- The neuroimmune interface in retinal regeneration.Progress in retinal and eye research · 2025Review
51 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 1 institution in 1 country.
Funding
Abstract
Chemokine (C-C motif) ligand 2 (CCL2), initially identified as monocyte chemoattractant protein-1 (MCP-1), recruits immune cells to the central nervous system (CNS) during autoimmune inflammation. CCL2 can be expressed by multiple cell types, but which cells are responsible for CCL2 function during acute and chronic phases of autoimmune disease is not known. We determined the role of CCL2 in astrocytes in vivo during experimental autoimmune encephalomyelitis (EAE) by using Cre-loxP gene deletion. Mice with a conditional gene deletion of CCL2 from astrocytes had less severe EAE late in disease while having a similar incidence and severity of disease at onset as compared to wild type (WT) control littermates. EAE mice devoid of CCL2 in astrocytes had less macrophage and T cell inflammation in the white matter of the spinal cord and less diffuse activation of astrocytes and microglia in both white and gray matter as well as less axonal loss and demyelination, compared to WT littermates. These findings demonstrate that CCL2 in astrocytes plays an important role in the continued recruitment of immune cells and activation of glial cells in the CNS during chronic EAE, thereby suggesting a novel cell specific target for neuroprotective treatments of chronic neuroinflammatory diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.