There are wider implications of the treatments described by Sharma et al.1 Bortezomib works by promoting apoptosis in long-lived and short-lived plasma cells responsible for long-lived immunity. These cells produce background levels of vaccine-induced protective antibodies. Therefore, there may be reduced titers of immunoglobulins against measles, mumps, and tetanus after bortezomib treatment of systemic lupus erythematosus.2 Bortezomib is now also considered treatment in many antibody-mediated chronic autoimmune diseases. It may provide a rapid reduction in antibody titers in treatment-refractory neurologic antibody–mediated diseases, such as NMDAR encephalitis, if standard immunotherapies are ineffective.3 Standard immunotherapies, such as methylprednisolone, rituximab, and cyclophosphamide, do not target these long-lived and short-lived plasma cells4; however, as some patients do not respond when these antibody-secreting cells are targeted, there is clearly more complexity to the immunopathogenesis than is currently understood.5 Neurologists should be aware of the potential pan-immunodeficient risks, particularly when it comes to vaccination-induced immunity, and also the potential therapeutic options in antibody-mediated neurologic conditions.
from Neurology recent issues http://bit.ly/2Wp5ZAW
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