Autoreactive B cells in Rheumatoid Arthritis / 中国免疫学杂志

ABSTRACT

Rheumatoid arthritis (RA) is an autoimmune disease characterized by the accumulation and proliferation of inflammatory cells in the synovial (joint) lining.By investigating RA pathologic processes and also through experimental models where immune complexes (inflammatory sediments) play a fundamental role.Many other autoantibodies have then come to our knowledge to be associated with the disease.Though it remains unknown the autoimmune pathology of B cells and why the clones of autoreactive B cells survive and proliferate in RA patients,but no doubt these autoantibodies represent a very useful tool in both diagnostic and prognostic terms.In joint synovial fulid,B cells also secrete cytokines,which can be interacted with other cells.B cells express IL-13 receptor a1 (IL-13Ra1),IL-13 can induce CD23 expression on B cells and promote proliferation of naive B cells. In addition,IL-13 is a cytokine which is produced mainly by activated T helper cell 2 (Th2 cells),it can inhibit the production of pro-inflammatory factor and chemokines,and has a certain relationship with the differentiation of B cells. Therefore,it is necessary to summarize the mechanims of RA pathogenesis related with B cells and IL-13,which has great significance in the diagnosis,treatment and basic immunology research of autoimmune diseases such as RA.