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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.
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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