ArticleBrain pathology (Zurich, Switzerland)2012
Deletion of beta-2-microglobulin ameliorates spinal cord lesion load and promotes recovery of brainstem NAA levels in a murine model of multiple sclerosis.
Article in Brain pathology (Zurich, Switzerland), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Proteomic analysis reveals candidate molecules to mediate cortical pathology and identify possible biomarkers in an animal model of multiple sclerosis.Frontiers in immunology · 2025Article
- When encephalitogenic T cells collaborate with microglia in multiple sclerosis.Nature reviews. Neurology · 2019Review
- Facets of Theiler's Murine Encephalomyelitis Virus-Induced Diseases: An Update.International journal of molecular sciences · 2019Review
- Antibody-Mediated Oligodendrocyte Remyelination Promotes Axon Health in Progressive Demyelinating Disease.Molecular neurobiology · 2016Review
- The Implication and Significance of Beta 2 Microglobulin: A Conservative Multifunctional Regulator.Chinese medical journal · 2016Review
- A single dose of a neuron-binding human monoclonal antibody improves brainstem NAA concentrations, a biomarker for density of spinal cord axons, in a model of progressive multiple sclerosis.Journal of neuroinflammation · 2015Article
- Deletion of Virus-specific T-cells Enhances Remyelination in a Model of Multiple Sclerosis.Journal of neurology & translational neuroscience · 2014Article
- Cuprizone-induced demyelination as a tool to study remyelination and axonal protection.Journal of molecular neuroscience : MN · 2013Review
- CD8(+) T cells in multiple sclerosis.Expert opinion on therapeutic targets · 2013Review
- Beta-2 microglobulin is important for disease progression in a murine model for amyotrophic lateral sclerosis.Frontiers in cellular neuroscience · 2013Article
- Preclinical (1)H-MRS neurochemical profiling in neurological and psychiatric disorders.Bioanalysis · 2012Review
- Neuronal expression of β2M and MHC I are essential for peripheral surveillance and targeting of neuron-restricted antigens.Frontiers in neurologyArticle
- Viral models of multiple sclerosis: neurodegeneration and demyelination in mice infected with Theiler's virus.Progress in neurobiologyArticle
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
We used genetic deletion of β2-microglobulin to study the influence of CD8(+) T cells on spinal cord demyelination, remyelination, axonal loss and brainstem N-acetyl aspartate levels during the acute and chronic phases of Theiler's murine encephalomyelitis virus (TMEV) infection. We used β2m(-/-) and β2m(+/+) B10.Q mice (of H-2(q) background) normally susceptible to TMEV-induced demyelination. Over the disease course, β2m(+/+) mice had increasing levels of demyelination and minimal late-onset remyelination. In contrast, β2m(-/-) mice had steady levels of demyelination from 45-390 dpi and remyelination was extensive and more complete. Early in the disease, brainstem NAA levels drop in both strains, but accordingly with remyelination and axonal preservation, NAA recover in β2m(-/-) mice despite equivalent brainstem pathology. At 270 dpi, β2m(+/+) mice had significantly fewer spinal cord axons than β2m(-/-) mice (up to 28% less). In addition, β2m(+/+) mice lost axons of all calibers, whereas β2m(-/-) mice had a modest loss of only medium- and large-caliber axons. This study further supports the hypothesis that CD8(+) T cells are involved in demyelination, and axonal loss following Theiler's virus-induced demyelination.
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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.