HLA-B27-associated reactive arthritis: pathogenetic and clinical considerations.
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, non-culturable 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.
Colmegna
Inés
I
Section of Rheumatology, Department of Medicine, LSU Health Science Center, New Orleans, Louisiana 70112, USA.
Cuchacovich
Raquel
R
Espinoza
Luis R
LR
D000818:Animals; D016918:Arthritis, Reactive / Q000175:diagnosis / Q000453:epidemiology / Q000382:microbiology / Q000503:physiopathology / Q000628:therapy; D002689:Chlamydia / Q000302:isolation & purification; D004755:Enterobacteriaceae / Q000302:isolation & purification; D016905:Gram-Negative Bacterial Infections / Q000150:complications; D015796:HLA-B27 Antigen / Q000235:genetics / Q000378:metabolism; D006801:Humans; D051379:Mice; D000091402:Prohibitins; D051381:Rats
D015796:HLA-B27 Antigen; C000717331:PHB2 protein, human; D000091402:Prohibitins