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Rituximab
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==Mode of action== Rituximab works in autoimmune disease by destroying memory B cells committed to producing autoantibodies that cause symptoms and signs of disease.The drug binds to the surface of the B cell by attaching to the CD20 molecule. This triggers cell death through several mechanisms including antibody dependent cytotoxicity and apoptosis. If the drug is infused slowly, B cells are removed without causing any unpleasant symptoms. Rituximab cannot target autoreactive cells specifically so it leads to depletion of memory B cells as a whole. This is probably not associated with major immunosuppression because antibodies to microbes are mostly made by long lived plasma cells derived in the past from memory B cells and these are not targeted by rituximab. Autoantibodies appear often to be produced by shorter lived plasma cells which die off rapidly. B cell depletion with rituximab tends to last about 6 months. After that, when B cells return some patients will suffer an immediate relapse of autoimmune symptoms but others may continue well for a period of months or years and for some conditions apparently long term. So far it is unclear whether or not any effect in ME/CFS can continue long term or whether repeated treatment will be required, as is the case, for instance, for rheumatoid arthritis.
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