Background
Accumulating data indicate that bone marrow (BM) in rheumatoid arthritis (RA) patients participates in the pathogenesis of RA as a site of proinflammatory cytokine overproduction, lymphocyte homing and cell activation. IL-1b, IL-6, TNFα and IL-15 are among the proinflammatory cytokines elevated in RA in comparison with osteoarthritis (OA) patient BM. At present, it is unclear why the RA BM microenvironment produces more proinflammatory cytokines than OA BM. One possibility is that, in addition to physiological production, exogenous and/or endogenous factors further enhance innate immune responses in RA BM. Importantly, our recent data indicate that RA BM-derived B cells express functional Toll-like receptor 9 (TLR9), and therefore could respond to TLR9 agonist stimulation.