ArticleNeurology(R) neuroimmunology & neuroinflammation2022
Siponimod Inhibits the Formation of Meningeal Ectopic Lymphoid Tissue in Experimental Autoimmune Encephalomyelitis.
Article in Neurology(R) neuroimmunology & neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 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
16 citing papers in PubMed, 19 citations in OpenAlex.
- Insights and challenges on animal models for progressive multiple sclerosis.Journal of neuroinflammation · 2026Review
- Tertiary Lymphoid Structures Across Organs: Context, Composition, and Clinical Levers.Immunological reviews · 2025Review
- Review
- High efficacy therapy to prevent the formation of meningeal tertiary lymphoid organs after CXCL13 index screening in early multiple sclerosis.Frontiers in neuroscience · 2025Article
- Tertiary Lymphoid Structures in Central Nervous System Disorders.Methods in molecular biology (Clifton, N.J.) · 2025Review
- CXCL13 as a Biomarker: Background and Utility in Multiple Sclerosis.Biomolecules · 2024Review
- Siponimod treatment response shows partial BDNF dependency in multiple sclerosis models.Scientific reports · 2024Article
- Single-Cell Profiling Indicates a Proinflammatory Role of Meningeal Ectopic Lymphoid Tissue in Experimental Autoimmune Encephalomyelitis.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- Meningeal inflammation as a driver of cortical grey matter pathology and clinical progression in multiple sclerosis.Nature reviews. Neurology · 2023Review
- FirstTheranostics · 2023Article
- Impact of Siponimod on Enteric and Central Nervous System Pathology in Late-Stage Experimental Autoimmune Encephalomyelitis.International journal of molecular sciences · 2022Article
- A Review of Compartmentalised Inflammation and Tertiary Lymphoid Structures in the Pathophysiology of Multiple Sclerosis.Biomedicines · 2022Review
- Siponimod ameliorates metabolic oligodendrocyte injury via the sphingosine-1 phosphate receptor 5.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Breaching Brain Barriers: B Cell Migration in Multiple Sclerosis.Biomolecules · 2022Review
- Siponimod Inhibits the Formation of Meningeal Ectopic Lymphoid Tissue in Experimental Autoimmune Encephalomyelitis.Neurology(R) neuroimmunology & neuroinflammation · 2022Article
- Effects of a Fully Humanized Type II Anti-CD20 Monoclonal Antibody on Peripheral and CNS B Cells in a Transgenic Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesTo investigate whether the formation or retention of meningeal ectopic lymphoid tissue (mELT) can be inhibited by the sphingosine 1-phosphate receptor 1,5 modulator siponimod (BAF312) in a murine model of multiple sclerosis (MS).
methodsA murine spontaneous chronic experimental autoimmune encephalomyelitis (EAE) model, featuring meningeal inflammatory infiltrates resembling those in MS, was used. To prevent or treat EAE, siponimod was administered daily starting either before EAE onset or at peak of disease. The extent and cellular composition of mELT, the spinal cord parenchyma, and the spleen was assessed by histology and immunohistochemistry.
resultsSiponimod, when applied before disease onset, ameliorated EAE. This effect was also present, although less prominent, when treatment started at peak of disease. Treatment with siponimod resulted in a strong reduction of the extent of mELT in both treatment paradigms. Both B and T cells were diminished in the meningeal compartment. DISCUSSION: Beneficial effects on the disease course correlated with a reduction in mELT, suggesting that inhibition of mELT may be an additional mechanism of action of siponimod in the treatment of EAE. Further studies are needed to establish causality and confirm this observation in MS.
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.