ReviewCNS drugs2018
Impact of Glatiramer Acetate on B Cell-Mediated Pathogenesis of Multiple Sclerosis.
Review in CNS drugs, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 34 citations in OpenAlex.
- Repopulation of T, B, and NK cells following alemtuzumab treatment in relapsing-remitting multiple sclerosis.Journal of neuroinflammation · 2020Trial
- Trial
- T Helper Cells and Cytokine Networks in the Immunopathogenesis of Multiple Sclerosis.ImmunoTargets and therapy · 2026Review
- SPI1 triggers the formation of neutrophil extracellular traps in multiple sclerosis through CXCL4.Journal of molecular histology · 2025Article
- Glatiramer Acetate Modifies the Immune Profiles of Monocyte-Derived Dendritic Cells In Vitro Without Affecting Their Generation.International journal of molecular sciences · 2025Article
- A narrative review on the safety of glatiramer acetate in multiple sclerosis: focus on Europe.Therapeutic advances in chronic disease · 2025Review
- Glatiramer acetate in situ forming gel, a new approach for multiple sclerosis treatment.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2024Article
- Disease Modifying Strategies in Multiple Sclerosis: New Rays of Hope to Combat Disability?Current neuropharmacology · 2024Review
- Synapse Dysfunctions in Multiple Sclerosis.International journal of molecular sciences · 2023Review
- Serum levels of IgM to phosphatidylcholine predict the response of multiple sclerosis patients to natalizumab or IFN-β.Scientific reports · 2022Article
- Blood-brain barrier: emerging trends on transport models and new-age strategies for therapeutics intervention against neurological disorders.Molecular brain · 2022Review
- Review
- EBV-specific CD8 T lymphocytes and B cells during glatiramer acetate therapy in patients with MS.Neurology(R) neuroimmunology & neuroinflammation · 2020Article
- Differential Effects of MS Therapeutics on B Cells-Implications for Their Use and Failure in AQP4-Positive NMOSD Patients.International journal of molecular sciences · 2020Review
- Article
- A case of Disseminated Herpes Zoster in a patient with Multiple Sclerosis on Glatiramer acetate.IDCases · 2020Article
- Immunological Aspects of Approved MS Therapeutics.Frontiers in immunology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growing evidence indicates that B cells play a key role in the pathogenesis of multiple sclerosis (MS). B cells occupy distinct central nervous system (CNS) compartments in MS, including the cerebrospinal fluid and white matter lesions. Also, it is now known that, in addition to entering the CNS, B cells can circulate into the periphery via a functional lymphatic system. Data suggest that the role of B cells in MS mainly involves their in situ activation in demyelinating lesions, leading to altered pro- and anti-inflammatory cytokine secretion, and a highly effective antigen-presenting cell function, resulting in activation of memory or naïve T cells. Clinically, B cell-depleting agents show significant efficacy in MS. In addition, many disease-modifying therapies (DMTs) traditionally understood to target T cells are now known to influence B cell number and function. One of the earliest DMTs to be developed, glatiramer acetate (GA), has been shown to reduce the total frequency of B cells, plasmablasts, and memory B cells. It also appears to promote a shift toward reduced inflammation by increasing anti-inflammatory cytokine release and/or reducing pro-inflammatory cytokine release by B cells. In the authors' opinion, this may be mediated by cross-reactivity of B cell receptors for GA with antigen (possibly myelin basic protein) expressed in the MS lesion. More research is required to further characterize the role of B cells and their bidirectional trafficking in the pathogenesis of MS. This may uncover novel targets for MS treatments and facilitate the development of B cell biomarkers of drug response.
Indexed as
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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.