HLA-B27-Associated Reactive Arthritis: Pathogenetic and Clinical Considerations

AUTOR(ES)

Colmegna, Inés

FONTE

American Society for Microbiology

RESUMO

Current evidence supports the concept that reactive arthritis (ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable, nonculturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body. The mechanisms that lead to the development of ReA are complex and basically involve an interaction between an arthritogenic agent and a predisposed host. The way in which a host accommodates to invasive facultative intracellular bacteria is the key to the development of ReA. The details of the molecular pathways that explain the articular and extra-articular manifestations of the disease are still under investigation. Several studies have been done to gain a better understanding of the pathogenesis of ReA; these constitute the basis for a more rational therapeutic approach to this disease.

Documentos Relacionados

• Endogenous Processing and Presentation of T-cell Epitopes from Chlamydia trachomatis with Relevance in HLA-B27-associated Reactive Arthritis*
• HLA-B27 and the causes of arthritis: does molecular biology help?
• IgG and IgA immune response against klebsiella in HLA-B27-associated anterior uveitis.
• HLA-B27 associated reactive spondyloarthropathies in a Dutch military hospital.
• Isolated HLA-B27 cross reactive group (CREG) associated Achilles tendinitis.