Epstein–Barr Virus in Multiple Sclerosis: Theory and Emerging Immunotherapies
Amit Bar‐Or, Michael P. Pender, Rajiv Khanna, Lawrence Steinman, Hans‐Peter Hartung, Tap Maniar, Ed Croze, Blake T. Aftab, Gavin Giovannoni, Manher Joshi
Abstract
In our above review there is an error at the bottom of Figure 1 on the left: the text insert “Co-stimulatory survival signals (CD28-B7) inhibit T cell apoptosis allowing interaction with antigen-presenting cells (astrocytes/microglia)” should be replaced with “Co-stimulatory survival signals (B7) produced by EBV-infected B cells inhibit T cell apoptosis, allowing survival of autoreactive T cells”. Original Figure 1 The text insert “Co-stimulatory survival signals (CD28-B7) inhibit T cell apoptosis allowing interaction with antigen-presenting cells (astrocytes/microglia)” should be replaced with “Co-stimulatory survival signals (B7) produced by EBV-infected B cells inhibit T cell apoptosis, allowing survival of autoreactive T cells” Epstein–Barr Virus in Multiple Sclerosis: Theory and Emerging ImmunotherapiesBar-Or et al.Trends in Molecular MedicineDecember 17, 2019In BriefNew treatments for multiple sclerosis (MS) focused on B cells have created an atmosphere of excitement in the MS community. B cells are now known to play a major role in disease, demonstrated by the highly impactful effect of a B cell-depleting antibody on controlling MS. The idea that a virus may play a role in the development of MS has a long history and is supported mostly by studies demonstrating a link between B cell-tropic Epstein–Barr virus (EBV) and disease onset. Efforts to develop antiviral strategies for treating MS are underway. Full-Text PDF Open Access