ArticleJournal of neuroimmunology2008
MHC class II exacerbates demyelination in vivo independently of T cells.
Article in Journal of neuroimmunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
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.
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Who cites it
41 citing papers in PubMed, 77 citations in OpenAlex.
- Niraparib Demonstrates Therapeutic Potential in Multiple Sclerosis through Inhibition of IL-17A Receptor Interaction and Promotion of Remyelination.ACS chemical neuroscience · 2025Article
- Zebrafish as a Model for Multiple Sclerosis.Biomedicines · 2024Review
- Meningeal lymphatic function promotes oligodendrocyte survival and brain myelination.Immunity · 2024Article
- p38γ MAPK delays myelination and remyelination and is abundant in multiple sclerosis lesions.Brain : a journal of neurology · 2024Article
- Immunoglobulin directly enhances differentiation of oligodendrocyte-precursor cells and remyelination.Scientific reports · 2023Article
- Imaging immunomodulatory treatment responses in a multiple sclerosis mouse model using hyperpolarizedCommunications medicine · 2023Article
- The Pathological Activation of Microglia Is Modulated by Sexually Dimorphic Pathways.International journal of molecular sciences · 2023Review
- Inhibiting microglia exacerbates the early effects of cuprizone in males in a rat model of multiple sclerosis, with no effect in females.Frontiers in neurology · 2023Article
- Single-cell microglial transcriptomics during demyelination defines a microglial state required for lytic carcass clearance.Molecular neurodegeneration · 2022Article
- 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
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- Animal models to investigate the effects of inflammation on remyelination in multiple sclerosis.Frontiers in molecular neuroscience · 2022Review
- Microglial Engulfment of Spines in the Ventral Zona Incerta Regulates Anxiety-Like Behaviors in a Mouse Model of Acute Pain.Frontiers in cellular neuroscience · 2022Article
- PART 2: Mouse models for multiple sclerosis research.Neurourology and urodynamics · 2021Review
- The Salvinorin Analogue, Ethoxymethyl Ether Salvinorin B, Promotes Remyelination in Preclinical Models of Multiple Sclerosis.Frontiers in neurology · 2021Article
- The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis.Cellular and molecular life sciences : CMLS · 2020Review
- The Cuprizone Model: Dos and Do Nots.Cells · 2020Review
- Article
- Molecular signature of different lesion types in the brain white matter of patients with progressive multiple sclerosis.Acta neuropathologica communications · 2019Article
- Systemic TLR2 tolerance enhances central nervous system remyelination.Journal of neuroinflammation · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We have shown previously the importance of MHC class II for central nervous system remyelination; however, the function of MHC class II during cuprizone-induced demyelination has not been examined. Here, we show that I-A(beta)-/- mice exhibit significantly reduced inflammation and demyelination. RAG-1(1/1) mice are indistinguishable from controls, indicating T cells may not play a role. The role of MHC class II depends on an intact cytoplasmic tail that leads to the production of IL-1beta, TNF-alpha, and nitric oxide, and oligodendrocyte apoptosis. Thus, the function of MHC class II cytoplasmic tail appears to increase microglial proliferation and activation that exacerbates 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.