2. Academic Validation
  3. A Tolerogenic Role of Cathepsin G in a Primate Model of Multiple Sclerosis: Abrogation by Epstein-Barr Virus Infection

A Tolerogenic Role of Cathepsin G in a Primate Model of Multiple Sclerosis: Abrogation by Epstein-Barr Virus Infection

  • Arch Immunol Ther Exp (Warsz). 2020 Jun 16;68(4):21. doi: 10.1007/s00005-020-00587-1.
Bert A 't Hart 1 2
Affiliations

Affiliations

  • 1 Department of Biomedical Sciences of Cells and Systems, University of Groningen, University Medical Center, Groningen, The Netherlands. mog3556@gmail.com.
  • 2 Department of Anatomy and Neurosciences, VU Medical Center, Amsterdam, The Netherlands. mog3556@gmail.com.
PMID: 32556812 DOI: 10.1007/s00005-020-00587-1
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.

Keywords

Antigen presentation; Autoimmune; B cells; EAE; Tolerance.

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