Disease mechanisms in reactive arthritis

Abstract

Reactive arthritis (ReA) occurs after a preceding bacterial infection of the urogenital or gastroenteral tract. The bacteria triggering ReA persist in vivo and seem to be responsible for triggering an immune response. A cytokine imbalance with a relative lack of T-helper 1 cytokines may play an important role allowing these bacteria to survive. This seems to be relevant for manifestation and chronicity of the arthritis. For the chronic cases and cases evolving into ankylosing spondylitis, the interaction between bacteria and human leukocyte antigen B27 plays an additional crucial role. Among others, the arthritogenic peptide hypothesis is one way to explain this association. Human leukocyte antigen B27-restricted peptides from Yersinia and Chlamydia, which are stimulatory for CD8+ T cells derived from patients with ReA, have been identified. The exact role of such peptides for the pathogenesis of ReA and other spondyloarthritides still has to be defined.