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Clinical Microbiology Reviews, April 2004, p. 348-369, Vol. 17, No. 2
0893-8512/04/$08.00+0     DOI: 10.1128/CMR.17.2.348-369.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

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

Section of Rheumatology, Department of Medicine, LSU Health Science Center, New Orleans, Louisiana 70112

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.

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