ReviewArchivum immunologiae et therapiae experimentalis2020
A Tolerogenic Role of Cathepsin G in a Primate Model of Multiple Sclerosis: Abrogation by Epstein-Barr Virus Infection.
Review in Archivum immunologiae et therapiae experimentalis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Role of autoreactive Tc17 cells in the pathogenesis of experimental autoimmune encephalomyelitis.Neuroprotection (Chichester, England) · 2024Article
- Understanding the link between neurotropic viruses, BBB permeability, and MS pathogenesis.Journal of neurovirology · 2024Review
- What do animal models tell us about the role of EBV in the pathogenesis of multiple sclerosis?Frontiers in immunology · 2022Review
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Authors and funding
1 author.
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Abstract
Using a non-human primate model of the autoimmune neuroinflammatory disease multiple sclerosis (MS), we have unraveled the role of B cells in the making and breaking of immune tolerance against central nervous system myelin. It is discussed here that B cells prevent the activation of strongly pathogenic T cells present in the naïve repertoire, which are directed against the immunodominant myelin antigen MOG (myelin oligodendrocyte glycoprotein). Prevention occurs via destructive processing of a critical epitope (MOG34-56) through the lysosomal serine protease cathepsin G. This effective tolerance mechanism is abrogated when the B cells are infected with Epstein-Barr virus, a ubiquitous γ1-herpesvirus that entails the strongest non-genetic risk factor for MS.
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