Reactive arthritis （ReA）, also known as sterile postin-fectious arthritis, belongs to the group of related ar-thropathies known as spondyloarthritis （SpA）. ReA can arise 1-4 wk after a gastrointestinal or genitour...Reactive arthritis （ReA）, also known as sterile postin-fectious arthritis, belongs to the group of related ar-thropathies known as spondyloarthritis （SpA）. ReA can arise 1-4 wk after a gastrointestinal or genitourinary infection, but once arthritis develops, the microorgan-ism is not found in the joint. The classical microbes as-sociated with ReA development include Gram-negative aerobic or microaerophilic bacteria containing LPS in their outer membrane. The immunopathogenic mechanisms involved in ReA development are still unknown. A hypothesis suggested that the bacteria probably persist outside the joint, at sites such as gut mucosa or lymph nodes, and bacterial antigens might then be transported to the joints. On the other hand, an altered immune response and the unbalanced production of cy-tokines have been reported in subjects with ReA. Currently, there is increased evidence to suggest that both mechanisms would operate in the immunopathogenesis of ReA. In this review we highlight recent advances on the role of cytokines in the ReA. Particularly, we discuss the roles of some pro- and anti-infammatory cytokines involved in the immunopathogenesis of ReA.展开更多
基金Supported by Agencia Nacional de Promoción Científica y Tecnológica,No.PICT 2008-763,PICT 2011-732by the National University of San Luis(Project 0401)+1 种基金by the Scientific Career of National Council of Scientific and Technical Investigationsby National Council of Scientific and Technical Investigations
文摘Reactive arthritis （ReA）, also known as sterile postin-fectious arthritis, belongs to the group of related ar-thropathies known as spondyloarthritis （SpA）. ReA can arise 1-4 wk after a gastrointestinal or genitourinary infection, but once arthritis develops, the microorgan-ism is not found in the joint. The classical microbes as-sociated with ReA development include Gram-negative aerobic or microaerophilic bacteria containing LPS in their outer membrane. The immunopathogenic mechanisms involved in ReA development are still unknown. A hypothesis suggested that the bacteria probably persist outside the joint, at sites such as gut mucosa or lymph nodes, and bacterial antigens might then be transported to the joints. On the other hand, an altered immune response and the unbalanced production of cy-tokines have been reported in subjects with ReA. Currently, there is increased evidence to suggest that both mechanisms would operate in the immunopathogenesis of ReA. In this review we highlight recent advances on the role of cytokines in the ReA. Particularly, we discuss the roles of some pro- and anti-infammatory cytokines involved in the immunopathogenesis of ReA.
