Rheumatoid arthritis (RA) is an autoimmune disease epitomized by severe inflammation that induces tendon, cartilage, and bone damage over time. Although different types of cells undertake pathogenic functions in RA, the B cell's significant involvement has increasingly been known following the development of rheumatoid factor and it has been re-emphasized in recent years. Therefore, the rheumatoid factors and anti-cyclic citrullinated peptide antibodies are well-known indications of infection and clinical manifestations, and that they can precede the development of illness by several years. The emergence of rituximab a B cell reducing chimeric antidote in 1997 and 1998 transformed B-cell-targeted therapy for inflammatory disorder from a research hypothesis to a functional fact. Ever since, several autoantibody-related conditions were addressed, including the more intriguing indications of effectiveness seen in rheumatoid arthritis patients. Numerous types of B-cell-targeted compounds are currently being researched. From the beginning, one of the primary goals of B-cell therapy was to reinstate some kind of immune tolerance. While B cells have long been recognized as essential autoantibody producers, certain antibody-independent functions and usefulness as a key targeted therapy were not recognized until recently. The knowledge of B cells' diverse physical and pathogenic roles in autoimmune diseases is growing. As a result, the number of successful agents targeting the B cell complex is becoming more ubiquitous. Therefore, in this article, we explore fresh perspectives upon the roles of B cells in arthritis treatment, as well as new evidence regarding the effectiveness of B lymphocytes reduction and the therapeutic outcome of biological markers.
Keywords: B cell depletion therapy; B cells; Rheumatoid arthritis; Rituximab.
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