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.
Original language | English |
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Article number | 21 |
Journal | Archivum immunologiae et therapiae experimentalis |
Volume | 68 |
Issue number | 4 |
DOIs | |
Publication status | Published - 1 Aug 2020 |
Keywords
- Antigen presentation
- Autoimmune
- B cells
- EAE
- Tolerance