Abstract
Rituximab, a monoclonal antibody targeting the B cell marker CD20, was initially approved in 1997 by the United States Food and Drug Administration (FDA) for the treatment of non-Hodgkin lymphoma. Since that time, rituximab has been FDA-approved for rheumatoid arthritis and vasculitides, such as granulomatosis with polyangiitis and microscopic polyangiitis. Additionally, rituximab has been used off-label in the treatment of numerous other autoimmune diseases, with notable success in pemphigus, an autoantibody-mediated skin blistering disease. The efficacy of rituximab therapy in pemphigus has spurred interest in its potential to treat other autoantibody-mediated diseases. This review summarizes the efficacy of rituximab in pemphigus and examines its off-label use in other select autoantibody-mediated diseases.
Highlights
Autoimmunity occurs when the body’s immune system mistakenly attacks self rather than foreign pathogens, leading to end-organ damage
Rituximab has striking efficacy in pemphigus, a finding mostly attributed to the central role of autoreactive B cells and autoantibodies in this disease
Rituximab has been shown to downregulate autoreactive T helper cells in pemphigus patients, either by reducing B-cell-mediated antigen presentation or through direct depletion of CD20+ T cells; the latter has been identified at similar rare frequencies in patients with multiple sclerosis and rheumatoid arthritis and in healthy individuals their pathophysiologic significance to disease onset and remission after rituximab remains unclear[1,2,3]
Summary
F1000 Faculty Reviews are written by members of the prestigious F1000 Faculty. They are commissioned and are peer reviewed before publication to ensure that the final, published version is comprehensive and accessible. The reviewers who approved the final version are listed with their names and affiliations. Any comments on the article can be found at the end of the article
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