Abstract

Anti-citrullinated protein antibodies are a hallmark of rheumatoid arthritis. It is widely acknowledged that the presence of ACPAs is the result of the interaction of genes, the environment and epigenetic modifications. The mechanism by which the factors, especially citrullination and ACPA glycosylation, affect ACPAs is still unclear. In this article, we review the presence of the ACPAs in RA and their relationship with clinical manifestations. The pathogenicity of ACPAs and B cells in RA was also summarized. A growing body of evidence has shown that ACPA-positive patients have more serious bone erosion and destruction and poor clinical prognosis than ACPA-negative patients. Recently, with the direct study of citrullinated protein-reactive B cells, their role in the development of rheumatoid arthritis has been further understood. It indicates that further understanding of the mechanism of ACPAs and CP-reactive B cells would beneficial in the prevention and treatment of RA.

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