ReviewFrontiers in immunology2017
CCL5-Glutamate Cross-Talk in Astrocyte-Neuron Communication in Multiple Sclerosis.
Review in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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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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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.
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Who cites it
44 citing papers in PubMed, 78 citations in OpenAlex.
- Comparative Analysis of Mouse CSF Proteins in Experimental Autoimmune Encephalomyelitis Model and Cuprizone-Induced Demyelination Model by Olink Proteomics.Molecular neurobiology · 2026Article
- Pathological Characteristics of the Lung and Brain in Cotton Rats and BALB/c Mice Infected with Respiratory Syncytial Virus.Viruses · 2026Article
- The Role of the CCR5 Receptor in Neuropathic Pain Modulation: Current Insights and Therapeutic Implications.Biomedicines · 2025Review
- Addressing neuroinflammation in human induced pluripotent stem cell-derived central nervous system neurospheroids.iScience · 2025Article
- Systematic Analysis of Alternative Splicing in Transcriptomes of Multiple Sclerosis Patient Brain Samples.International journal of molecular sciences · 2025Article
- Human Brain Organoids: A New Model to StudyJournal of fungi (Basel, Switzerland) · 2025Article
- IL-1ra and CCL5, but not IL-10, are promising targets for treating SMA astrocyte-driven pathology.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Exploring neuroglial signaling: diversity of molecules implicated in microglia-to-astrocyte neuroimmune communication.Reviews in the neurosciences · 2025Review
- DMH1-loaded peptide nanomicelles restore myelin and attenuate neuroinflammation in trigeminal neuralgia via CCL5 suppression.Frontiers in pharmacology · 2025Article
- Perioperative changes in inflammatory biomarkers and underlying molecular mechanisms in patients with trigeminal neuralgia undergoing surgical interventions.Frontiers in neurology · 2025Review
- Non-canonical Roles of Complement in the CNS: From Synaptic Organizer to Presynaptic Modulator of Glutamate Transmission.Current neuropharmacology · 2025Review
- Molecular Role of HIV-1 Human Receptors (CCL5-CCR5 Axis) in neuroAIDS: A Systematic Review.Microorganisms · 2024Review
- Comparison of Cytokine RANTES/CCL5 Inflammation in Apical Periodontitis and in Jawbone Cavitations - Retrospective Clinical Study.Journal of inflammation research · 2024Article
- Heightened presence of inflammatory mediators in the cerebrospinal fluid of patients with trigeminal neuralgia.Pain reports · 2023Article
- Article
- SAFit2 ameliorates paclitaxel-induced neuropathic pain by reducing spinal gliosis and elevating pro-resolving lipid mediators.Journal of neuroinflammation · 2023Article
- CCL5/CCR5-mediated peripheral inflammation exacerbates blood‒brain barrier disruption after intracerebral hemorrhage in mice.Journal of translational medicine · 2023Article
- Transport of the Proinflammatory Chemokines C-C Motif Chemokine Ligand 2 (MCP-1) and C-C Motif Chemokine Ligand 5 (RANTES) across the Intact Mouse Blood-Brain Barrier Is Inhibited by Heparin and Eprodisate and Increased with Systemic Inflammation.The Journal of pharmacology and experimental therapeutics · 2023Article
- Presynaptic 5-HTCells · 2022Article
- MicroRNA: A Linking between Astrocyte Dysfunction, Mild Cognitive Impairment, and Neurodegenerative Diseases.Life (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immune system (IS) and the central nervous system (CNS) are functionally coupled, and a large number of endogenous molecules (i.e., the chemokines for the IS and the classic neurotransmitters for the CNS) are shared in common between the two systems. These interactions are key elements for the elucidation of the pathogenesis of central inflammatory diseases. In recent years, evidence has been provided supporting the role of chemokines as modulators of central neurotransmission. It is the case of the chemokines CCL2 and CXCL12 that control pre- and/or post-synaptically the chemical transmission. This article aims to review the functional cross-talk linking another endogenous pro-inflammatory factor released by glial cells, i.e., the chemokine Regulated upon Activation Normal T-cell Expressed and Secreted (CCL5) and the principal neurotransmitter in CNS (i.e., glutamate) in physiological and pathological conditions. In particular, the review discusses preclinical data concerning the role of CCL5 as a modulator of central glutamatergic transmission in healthy and demyelinating disorders. The CCL5-mediated control of glutamate release at chemical synapses could be relevant either to the onset of psychiatric symptoms that often accompany the development of multiple sclerosis (MS), but also it might indirectly give a rationale for the progression of inflammation and demyelination. The impact of disease-modifying therapies for the cure of MS on the endogenous availability of CCL5 in CNS will be also summarized. We apologize in advance for omission in our coverage of the existing literature.
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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.