ArticleNature medicine1998
Absence of neurological deficits following extensive demyelination in a class I-deficient murine model of multiple sclerosis.
Article in Nature medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
79 citing papers in PubMed, 198 citations in OpenAlex.
- IgA Deficiency Exacerbates an Animal Model of Multiple Sclerosis Induced with Theiler's Virus.Cells · 2026Article
- CLEC12A signaling represses protective immune responses and contributes to hippocampal pathology in neurotropic picornavirus infection.Scientific reports · 2025Article
- CXCL13 as a Biomarker: Background and Utility in Multiple Sclerosis.Biomolecules · 2024Review
- Exploring the Role of Platelets in Virus-Induced Inflammatory Demyelinating Disease and Myocarditis.International journal of molecular sciences · 2024Article
- Ovalbumin-specific CD4Frontiers in immunology · 2023Article
- Remyelination in animal models of multiple sclerosis: finding the elusive grail of regeneration.Frontiers in molecular neuroscience · 2023Review
- Critical role of TLR activation in viral replication, persistence, and pathogenicity of Theiler's virus.Frontiers in immunology · 2023Review
- Curdlan, a Microbial β-Glucan, Has Contrasting Effects on Autoimmune and Viral Models of Multiple Sclerosis.Frontiers in cellular and infection microbiology · 2022Article
- Double-edged effects of tamoxifen-in-oil-gavage on an infectious murine model for multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2021Article
- Excessive Innate Immunity Steers Pathogenic Adaptive Immunity in the Development of Theiler's Virus-Induced Demyelinating Disease.International journal of molecular sciences · 2021Review
- Facets of Theiler's Murine Encephalomyelitis Virus-Induced Diseases: An Update.International journal of molecular sciences · 2019Review
- Cytotoxic CD8Brain pathology (Zurich, Switzerland) · 2018Article
- Multiple Sclerosis: Mechanisms of Disease and Strategies for Myelin and Axonal Repair.Neurologic clinics · 2018Review
- Multiple sclerosis: experimental models and reality.Acta neuropathologica · 2017Review
- Major histocompatibility complex class I molecules protect motor neurons from astrocyte-induced toxicity in amyotrophic lateral sclerosis.Nature medicine · 2016Article
- Th17-biased RORγt transgenic mice become susceptible to a viral model for multiple sclerosis.Brain, behavior, and immunity · 2015Article
- Deletion of Virus-specific T-cells Enhances Remyelination in a Model of Multiple Sclerosis.Journal of neurology & translational neuroscience · 2014Article
- Axons are injured by antigen-specific CD8(+) T cells through a MHC class I- and granzyme B-dependent mechanism.Neurobiology of disease · 2013Article
- CD8(+) T cells in multiple sclerosis.Expert opinion on therapeutic targets · 2013Review
- Deletion of beta-2-microglobulin ameliorates spinal cord lesion load and promotes recovery of brainstem NAA levels in a murine model of multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2012Article
19 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
6 authors at 1 institution in 1 country.
Funding
Abstract
Demyelination alone has been considered sufficient for development of neurological deficits following central nervous system (CNS) disease. However, extensive demyelination is not always associated with clinical deficits in patients with multiple sclerosis (MS), the most common primary demyelinating disease in humans. We used the Theiler's murine encephalomyelitis virus model of demyelination to investigate the role of major histocompatibility complex (MHC) class I and class II gene products in the development of functional and neurophysiological deficits following demyelination. We measured spontaneous clinical activity by two independent assays and recorded hind-limb motor-evoked potentials in infected class I-deficient and class II-deficient mice of an identical genetic background as well as in highly susceptible SJL/J mice. The results show that despite a similar distribution and extent of demyelinated lesions in all mice, only class I-deficient mice were functionally normal. We propose that the mechanism by which demyelinated class I-deficient mice maintain neurologic function results from increased sodium channel densities and the relative preservation of axons. These findings are the first to implicate a role for MHC class I in the development of neurological deficits following demyelination.
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.