Context
Although joint destruction is a complication of severe rheumatoid arthritis (RA), the definitive pathogenic mechanisms have yet to be elucidated. TRANCE/RANKL has been characterized as an essential factor not only for osteoclastogenesis, but also for the viability of dendritic cells resulting in the activation and proliferation of T cells. A significant reduction of bone erosion is seen in the adjuvant arthritis model after blockade of TRANCE/RANKL. To exclude the influence of T cell-dendritic cell interactions on this process, the authors generated inflammatory arthritis in TRANCE/RANKL-deficient mice using a serum transfer model bypassing the requirement for T cell activation.