scholarly journals Posttransplant Lymphoproliferative Disease in Primary Epstein‐Barr Virus Infection after Liver Transplantation: The Role of Cytomegalovirus Disease

1997 ◽  
Vol 176 (6) ◽  
pp. 1462-1467 ◽  
Author(s):  
Rafael Mañez ◽  
Mary C. Breinig ◽  
Peter Linden ◽  
John Wilson ◽  
Julian Torre‐Cisneros ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Epstein Barr Virus ◽  
Lymphoproliferative Disease ◽  
Epstein Barr Virus Infection ◽  
Cytomegalovirus Disease ◽  
Barr Virus ◽  
Posttransplant Lymphoproliferative Disease ◽  
Epstein Barr ◽  
Barr Virus Infection

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

2020 ◽  
Vol 68 (4) ◽  
Author(s):  
Bert A. ‘t Hart
Keyword(s):  
Multiple Sclerosis ◽  
B Cells ◽  
Epstein Barr Virus ◽  
Cathepsin G ◽  
Epstein Barr Virus Infection ◽  
Primate Model ◽  
Barr Virus ◽  
Epstein Barr ◽  
Barr Virus Infection

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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