ArticleJournal of neuroimmunology2013
Myelin antigen load influences antigen presentation and severity of central nervous system autoimmunity.
Article in Journal of neuroimmunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Roles in Innate Immunity.Advances in neurobiology · 2024Review
- Article
- Phenotypic characterization of a Csf1r haploinsufficient mouse model of adult-onset leukodystrophy with axonal spheroids and pigmented glia (ALSP).Neurobiology of disease · 2015Article
- Retinal antigen-specific regulatory T cells protect against spontaneous and induced autoimmunity and require local dendritic cells.Journal of neuroinflammation · 2014Article
- Fasudil regulates T cell responses through polarization of BV-2 cells in mice experimental autoimmune encephalomyelitis.Acta pharmacologica Sinica · 2014Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
This study was designed to understand the impact of self-antigen load on manifestation of organ specific autoimmunity. Using a transgenic mouse model characterized by CNS hypermyelination, we show that larger myelin content results in greater severity of experimental autoimmune encephalomyelitis attributable to an increased number of microglia within the hypermyelinated brain. We conclude that a larger self-antigen load affects an increase in number of tissue resident antigen presenting cells (APCs) most likely due to compensatory antigen clearance mechanisms thereby enhancing the probability of productive T cell-APC interactions in an antigen abundant environment and results in enhanced severity of autoimmune disease.
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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.