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Abstract
The mechanisms leading to the development of HLA-B27-associated diseases, spondyloarthropathies, are unknown. One of them, reactive arthritis, is clearly caused by an infection, and joint inflammation develops soon after or during an infection elsewhere in the body. In other forms of spondyloarthropathies, such as ankylosing spondylitis, association with infection is suggested but it is not as clear. Pathogenetic mechanisms of reactive arthritis are a focus of great interest as causative infections and strong genetic association are known. How HLA-B27 determines the appearance of joint complications after certain infections is not clear. Several theories have been proposed to explain the association, and they usually include the idea that interaction between microbe and host is abnormal and inefficient in HLA-B27-positive subjects in whom reactive arthritis develops.