Rituximab is often used as an “off-label” therapy in patients with immune-mediated neurological disorders (PIMND) including multiple sclerosis, autoimmune neuropathies, neuromyelitis optica, myasthenia gravis, paraneoplastic neurological disorders, and inflammatory myopathies. In the U.S., it is approved for the treatment of various B-cell driven malignancies, certain forms of vasculidites, and rheumatoid arthritis. Rituximab has been successfully used in the treatment of several diseases driven by B-cell dysregulation. Also, repletion rate of circulating and tissue levels of CD20 B-cells are variable. Tissue levels of CD20 expressing cells may be affected to a lesser degree than circulating CD20 cells. Rituximab causes short-term depletion of circulating naïve and memory B-cells through three main mechanisms: antibody-dependent cell mediated cytotoxicity, complement mediated cytotoxicity, and induction of apoptosis. Antagonism of CD20 by rituximab does not prevent B-cell regeneration nor does it affect plasmablast or plasma cell differentiation. CD20 is a cell surface antigen, which is expressed on pre-B cells, mature B cells and memory B cells ĬD20 is not expressed by hematopoietic stem cells and pro-B cells, and is subsequently lost upon terminal differentiation into plasma cells. Rituximab is a human-mouse monoclonal chimeric antibody that targets CD20 molecules, which are expressed by B-cells during their maturation. Given their central role in generating autoantibodies, they have become an important target for several autoimmune diseases. They are involved in antigen presentation, epitope specific autoantibody production, and cytokine production. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials.ī-cells play an important role in diverse autoimmune diseases, including neurological, connective tissue, and vasculitic disorders. There are no patents, products in development or marketed products to declare. Speaker fees: Genzyme, Teva, Novartis, Biogen, Mallinckrodt. Consultancy: Teva, Novartis, Genzyme, Biogen. P.R.: speaking fees, Bayer, Biogen Idec, Boehringer Ingelheim, Novartis, Merck Serono, Teva, Genzyme clinical trial steering committees, Novartis, Merck Serono. Speaking fees: Teva, Novartis, Biogen Idec. Grants: NIH, NINDS, NMSS (USA), Teva, Novartis, Biogen Idec, Genzyme, Roche, Genentech, Sanofi-Aventis, Acorda Therapeutics. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: All relevant data are within the paper and its Supporting Information files.įunding: The authors received no specific funding for this work.Ĭompeting interests: The authors have the following interests: Omar Khan consultancy: Teva, Biogen Idec, Genzyme, Novartis. Received: ApAccepted: DecemPublished: January 8, 2018Ĭopyright: © 2018 Memon et al. PLoS ONE 13(1):Įditor: Martin Sebastian Weber, Klinikum rechts der Isar der Technischen Universitat Munchen, GERMANY (2018) Long-term safety of rituximab induced peripheral B-cell depletion in autoimmune neurological diseases. Citation: Memon AB, Javed A, Caon C, Srivastawa S, Bao F, Bernitsas E, et al.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |