ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Lymphocryptovirus Infection of Nonhuman Primate B Cells Converts Destructive into Productive Processing of the Pathogenic CD8 T Cell Epitope in Myelin Oligodendrocyte Glycoprotein.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Epstein-Barr virus and multiple sclerosis: lesson learned to develop better nonhuman primate models.Experimental & molecular medicine · 2025Review
- Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025Review
- Autophagy pathways in autoimmune diseases.Journal of autoimmunity · 2023Review
- Universal or Personalized Mesenchymal Stem Cell Therapies: Impact of Age, Sex, and Biological Source.Cells · 2022Review
- Lysosomal peptidases-intriguing roles in cancer progression and neurodegeneration.FEBS open bio · 2022Review
- The Forgotten Brother: The Innate-like B1 Cell in Multiple Sclerosis.Biomedicines · 2022Review
- What do animal models tell us about the role of EBV in the pathogenesis of multiple sclerosis?Frontiers in immunology · 2022Review
- Mechanistic underpinning of an inside-out concept for autoimmunity in multiple sclerosis.Annals of clinical and translational neurology · 2021Review
- Viral infections and their relationship to neurological disorders.Archives of virology · 2021Review
- Bioorthogonal protein labelling enables the study of antigen processing of citrullinated and carbamylated auto-antigens.RSC chemical biology · 2021Article
- Synthesis of Asparagine Derivatives Harboring a Lewis X Type DC-SIGN Ligand and Evaluation of their Impact on Immunomodulation in Multiple Sclerosis.Chemistry (Weinheim an der Bergstrasse, Germany) · 2021Article
- Myelin-specific T cells in animals with Japanese macaque encephalomyelitis.Annals of clinical and translational neurology · 2021Article
- B Cell Metabolism and Autophagy in Autoimmunity.Frontiers in immunology · 2021Review
- A Tolerogenic Role of Cathepsin G in a Primate Model of Multiple Sclerosis: Abrogation by Epstein-Barr Virus Infection.Archivum immunologiae et therapiae experimentalis · 2020Review
- Animal Models for Gammaherpesvirus Infections: Recent Development in the Analysis of Virus-Induced Pathogenesis.Pathogens (Basel, Switzerland) · 2020Review
- Review
- Viral infections and multiple sclerosis.Drug discovery today. Disease models · 2020Review
- Autophagy in Multiple Sclerosis: Two Sides of the Same Coin.Frontiers in cellular neuroscience · 2020Review
- Review
- Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EBV is the major infectious environmental risk factor for multiple sclerosis (MS), but the underlying mechanisms remain obscure. Patient studies do not allow manipulation in vivo. We used the experimental autoimmune encephalomyelitis (EAE) models in the common marmoset and rhesus monkey to model the association of EBV and MS. We report that B cells infected with EBV-related lymphocryptovirus (LCV) are requisite APCs for MHC-E-restricted autoaggressive effector memory CTLs specific for the immunodominant epitope 40-48 of myelin oligodendrocyte glycoprotein (MOG). These T cells drive the EAE pathogenesis to irreversible neurologic deficit. The aim of this study was to determine why LCV infection is important for this pathogenic role of B cells. Transcriptome comparison of LCV-infected B cells and CD20(+) spleen cells from rhesus monkeys shows increased expression of genes encoding elements of the Ag cross-presentation machinery (i.e., of proteasome maturation protein and immunoproteasome subunits) and enhanced expression of MHC-E and of costimulatory molecules (CD70 and CD80, but not CD86). It was also shown that altered expression of endolysosomal proteases (cathepsins) mitigates the fast endolysosomal degradation of the MOG40-48 core epitope. Finally, LCV infection also induced expression of LC3-II(+) cytosolic structures resembling autophagosomes, which seem to form an intracellular compartment where the MOG40-48 epitope is protected against proteolytic degradation by the endolysosomal serine protease cathepsin G. In conclusion, LCV infection induces a variety of changes in B cells that underlies the conversion of destructive processing of the immunodominant MOG40-48 epitope into productive processing and cross-presentation to strongly autoaggressive CTLs.
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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.