Berek C
Deutsches Rheuma-Forschungszentrum, Schumannstr. 21-22, 10117 Berlin, Germany.
Z Rheumatol. 2005 Sep;64(6):383-8. doi: 10.1007/s00393-005-0779-4.
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.
B细胞在类风湿性关节炎(RA)发病机制中的作用长期以来一直存在争议。在此我们表明,受累关节中的慢性炎症会导致异位生发中心的形成。一种支持B细胞活化和分化的微环境得以建立。可能会产生浆细胞,它们将高亲和力的自身抗体直接分泌到滑膜组织中。抗原/抗体复合物的形成、补体级联反应的激活以及巨噬细胞的刺激可能会导致关节破坏。此外,B细胞是高效的抗原呈递细胞。它们似乎在滑膜T细胞的活化和细胞因子分泌的诱导中起关键作用。使用单克隆抗体利妥昔单抗进行B细胞清除疗法的成功进一步强调了B细胞在RA发病机制中的重要性。