Pathogenesis of reactive arthritis.

There is good evidence that bacteria persist in vivo in patients with reactive arthritis (ReA). While Chlamydia seem to hide inside the joint, other areas such as gut mucosa or lymph nodes seem to be more likely places for Salmonella and Yersinia. T-helper (Th) 1 cells secreting cytokines such as IFN gamma and TNF alpha are crucial for an effective elimination of these bacteria. An inhibited Th1-response could be demonstrated in ReA, probably contributing to bacterial persistence. While HLA-B27 is found in only approximately 50% of patients with acute ReA, HLA-B27 seems to be crucial for the development of features typical with chronic spondyloarthropathy, such as sacroiliitis. Among several hypotheses to explain the interaction of bacteria with HLA-B27, the most likely seems to be that until now unknown bacterial or self- antigens were presented by HLA-B27 to CD8(+) T-cells. An important site where the immunopathology takes place seems to be at the insertion of tendons and ligaments at bone. Because antibiotics have failed so far in the treatment of ReA immunomodulatory therapies, based on a better understanding of the pathogenesis, alone or in combination with antibiotics might be an option for the future.