Abstract
The role of B cells for the pathogenesis of rheumatoid arthritis (RA) has been debated for a long time. Here we show that chronic inflammation in the affected joints leads to the development of ectopic germinal centers. A micro-environment is established which supports B cell activation and differentiation. Plasma cells may develop which secrete autoantibodies of high affinity directly into the synovial tissue. Antigen/antibody complex formation, the activation of the complement cascade and the stimulation of macrophages may contribute to the destruction of joints. Furthermore, B cells are efficient antigen presenting cells. They seem to play a pivotal role in the activation of synovial T cells and the induction of cytokine secretion. The success of B cell depletion therapy by using the monoclonal antibody Rituximab further emphasized the importance of B cells in the pathogenesis of RA.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
