Rheumatoid arthritis (RA) is a common chronic autoimmune disease, and its pathogenesis remains to be fully elucidated. Recent evidences suggested that the abnormal count and the dysfunction of B cells played important roles in the development and progression of RA. B cells participate in the development and progression of RA through antibody dependent and independent pathways, and elucidating the specific molecular mechanisms of these pathways will provide new targets for the development of RA therapeutic drugs. This paper reviews the relationship between the B-cell dysfunction and the pathogenesis of RA, providing references for a comprehensive understanding of the pathogenesis of RA and exploring new therapeutic targets.