ReviewJournal of neuroinflammation2017
Regulatory T cells in multiple sclerosis and myasthenia gravis.
Review in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 178 papers, 3 of them syntheses that pooled it.
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
178 citing papers in PubMed, 3 syntheses or guidelines pooled it, 317 citations in OpenAlex.
- Myasthenia gravis and five autoimmune diseases: a bidirectional Mendelian randomization study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Pooled it
- Cross-syndrome: myasthenia gravis and the demyelinating diseases of the central nervous system combination. Systematic literature review and case reports.Acta neurologica Belgica · 2023Pooled it
- Efficacy of diet on fatigue, quality of life and disability status in multiple sclerosis patients: rapid review and meta-analysis of randomized controlled trials.BMC neurology · 2022Pooled it
- BCMA-directed mRNA CAR-T cell therapy for myasthenia gravis: exploratory biomarker analysis of a placebo-controlled phase 2b trial.Nature medicine · 2026Trial
- Safety and feasibility of intravenous fresh adipose-derived mesenchymal stem cells in secondary progressive multiple sclerosis: phase I/IIa clinical results.Stem cell research & therapy · 2026Trial
- The cGAS-STING Pathway: A Double-Edged Regulator of Neuroinflammation and Myelin Regeneration.Molecular neurobiology · 2026Review
- Mesenchymal stromal cells and neuroinflammation: a multimodal approach to neuroprotection and future therapeutic horizons.Translational neurodegeneration · 2026Review
- The role and mechanism of IL‑35 in myasthenia gravis (Review).International journal of molecular medicine · 2026Review
- Immunogenicity of Hepatitis B Virus Vaccination in Relapsing-Remitting Multiple Sclerosis Patients Under Immunocompromising Treatment.International journal of molecular sciences · 2026Observational
- TGF-β signaling mediates crosstalk between CD8Journal of biomedical science · 2026Article
- Associated Autoimmunity in Myasthenia Gravis in Denmark: A Nationwide Case-Control Study.European journal of neurology · 2026Article
- The ionotropic AMPA receptor contributes to autoimmunity via altered regulatory T cell differentiation.iScience · 2026Article
- Allogeneic MHC-mismatched microglia-like cell replacement as a therapeutic approach for multiple sclerosis.Journal of neuroinflammation · 2026Article
- Hsa_circ_0000313/miR-1224-3p/MKNK2 Axis Modulates CD4Mediators of inflammation · 2026Article
- Immunomodulatory and anti-inflammatory potential of S-nitrosoglutathione (GSNO) in multiple sclerosis: a review of mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Multiple sclerosis pathophysiology: a comprehensive review of genetic, environmental, and immunological drivers.Inflammopharmacology · 2025Review
- The Potential of β-Synuclein-Specific Regulatory T Cell Therapy as a Treatment for Progressive Multiple Sclerosis.International journal of molecular sciences · 2025Review
- LPX-TI641, a Tim3/4 Agonist, Induces Long-Term Immune Tolerance in Multiple Sclerosis Models.Pharmaceutics · 2025Article
- Immune Modulatory Effects of PD-1/PD-L1 in Myasthenia Gravis: Insights From Peripheral Blood Mononuclear Cell Analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Beyond the Surface: Investigating the Potential Mechanisms of Non-Motor Symptoms in Myasthenia Gravis.European journal of neurology · 2025Review
118 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is a chronic debilitating disease of the central nervous system primarily mediated by T lymphocytes with specificity to neuronal antigens in genetically susceptible individuals. On the other hand, myasthenia gravis (MG) primarily involves destruction of the neuromuscular junction by antibodies specific to the acetylcholine receptor. Both autoimmune diseases are thought to result from loss of self-tolerance, which allows for the development and function of autoreactive lymphocytes. Although the mechanisms underlying compromised self-tolerance in these and other autoimmune diseases have not been fully elucidated, one possibility is numerical, functional, and/or migratory deficits in T regulatory cells (Tregs). Tregs are thought to play a critical role in the maintenance of peripheral immune tolerance. It is believed that Tregs function by suppressing the effector CD4+ T cell subsets that mediate autoimmune responses. Dysregulation of suppressive and migratory markers on Tregs have been linked to the pathogenesis of both MS and MG. For example, genetic abnormalities have been found in Treg suppressive markers CTLA-4 and CD25, while others have shown a decreased expression of FoxP3 and IL-10. Furthermore, elevated levels of pro-inflammatory cytokines such as IL-6, IL-17, and IFN-γ secreted by T effectors have been noted in MS and MG patients. This review provides several strategies of treatment which have been shown to be effective or are proposed as potential therapies to restore the function of various Treg subsets including Tr1, iTr35, nTregs, and iTregs. Strategies focusing on enhancing the Treg function find importance in cytokines TGF-β, IDO, interleukins 10, 27, and 35, and ligands Jagged-1 and OX40L. Likewise, strategies which affect Treg migration involve chemokines CCL17 and CXCL11. In pre-clinical animal models of experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune myasthenia gravis (EAMG), several strategies have been shown to ameliorate the disease and thus appear promising for treating patients with MS or MG.
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.