EBV infected B cells drive destructive T cells ?


The remarkable clinical efficacy of anti-CD20 monoclonal antibodies (mAb) in relapsing-remitting multiple sclerosis points at the critical involvement of B cells in the disease. However, the exact pathogenic contribution of B cells is poorly understood. In this publication we review new data on the role of CD20+ B cells in a unique experimental autoimmune encephalomyelitis (EAE) model in common marmosets (Callithrix jacchus), a small-bodied neotropical primate (a rat-size monkey that looks like a Gizmo). We will also discuss the relevance of these data for MS. Different from rodent EAE models, but similar to MS, disease progression in marmosets can develop independent of autoantibodies (Nonsense from a group with a vested interest in development of primate EAE). Progressive disease is mediated by MHC class Ib (Caja-E) restricted cytotoxic T cells, which are activated by γ-herpesvirus-infected B cells and cause widespread demyelination of cortical gray matter. B-cell directed monoclonal antibody therapies (anti-CD20 versus anti-BLyS and anti-APRIL) have a variable effect on EAE progression, which we found associated with variable depletion of the Epstein Barr virus (EBV)-like γ-herpesvirus CalHV3 from lymphoid organs. These findings support an important pathogenic role of CD20+ B cell in MS, especially of the subset infected with EBV.

Epstein barr virus infects few species compared to humans. The marmoset is one of the few other species that can be infected by EBV. This study is suggesting that  viral infected B cells are acting as antigen presenting cells for destructive T cells. Is this relevant

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  • Is it not possible to reach a definitive conclusion about B cells and EBV? This theory has been doing the rounds for years. I'm 100% convinced that EBV in the CNS is the target of the immune attack. I can't believe that it's taking so long to prove it. Alemtuzumab has a major impact on depleting B cells which probably explain the huge reduction in relapses. Ocrelezumab does the same. Why can't the researchers join up the dots?
    PS I know Team G are examining this issue through the Charcot Project.

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