Background
Toll-like receptors (TLRs), a family of pathogen recognition receptors, represent an important component of the innate immune system that also contributes to the development of acquired immunity. TLR9 expressed in the cytoplasm of several cell types including B cells, and recognize and are activated by unmethylated CpG-rich, pathogen-derived DNA sequences. This CpG stimulation triggers B-cell proliferation and promotes Th1 response. Moreover, DNA containing CpG-rich motifs, acting as polyclonal stimuli, participates in the maintenance of serological memory by human memory B cells. Recent data indicate that bone marrow in rheumatoid arthritis (RA) patients may actively participate in the pathogenesis of RA as a secondary lymphoid organ via overproduction of proinflammatory cytokines and a site of effective antigen presentation.