Yersiniosis elicits both humoral and cell-mediated immune responses in the host. It appears that most of the antibody response is directed toward the lipopolysaccharide. Follow-up studies have, however, demonstrated that patients with Yersinia infection produce antibodies directed towards a multitude of antigenic determinants, both plasmid and chromo-somally encoded ones. The antibodies often persist for several months and in the case of postinfection complications even years. As yersiniosis is fairly common in some parts of the world it is thus not surprising that, for example in northern Europe, the sera of 10-30% of healthy blood donors indicate previous Y. enterocolitica or Y. pseudotuberculosis infection. A remarkable feature of Yersinia infection is that it may pass quite unnoticed. This is illustrated by occasional severe reactions upon transfusion of blood, the donor of which, unaware of it, has carried Yersinia in the blood. During preservation at refrigerator temperature the psychrophilic yersinias multiply. Furthermore, epidemiologic studies have demonstrated that many individuals with verifiable infection remain symptomless.
Reactive arthritis, a common postinfection complication of yersiniosis, belongs to the seronegative spondyloarthropathies strongly associated with possession of the class I major histocompatibility complex (MHC) antigen HLA-B27. Approximately 80% of patients with Yersinia-triggered reactive arthritis are B27-positive. Yersinia-triggered uveitis and urethritis are also associated with B27 antigens but erythema nodosum is not. Of the seronegative spondyloarthropathies, ankylosing spondylitis shows the strongest association to HLA-B27 (95%), and hypotheses regarding the pathogenesis of Yersinia-triggered reactive arthritis and ankylosing spondylitis go along similar lines. It has been suggested but not proven that molecular mimicry between antigens of the Yersinia microorganism and the B27 antigen leads to the development of reactive arthritis. Molecular mimicry might either cause ineffective elimination of the microorganism due to tolerance or, on the other hand, trigger autoimmunity. Extensive studies regarding the peptide-binding groove of the HLA-B27 molecule and of the bound peptides have not led to an explanation of this disease association. However, a surface component of Y. enterocolitica shares certain structural similarity with the human thyrotropin receptor.
There is evidence that patients with Yersinia-triggered reactive arthritis differ in their immune functions from yersiniosis patients with uncomplicated disease. The former tend to have a weaker Yersinia-specific cell-mediated immune response bur a stronger and more persistent immunoglobulin A (IgA) antibody response against the microbe. At the early phase of infection those with reactive arthritis show more Yersinia-sptcxhc opsonic antibodies, and they have more Yersmztf-specific immune complexes. In addition, B27-positive individuals may have exaggerated inflammatory responsiveness, such as stronger chemotactic function and production of some inflammatory mediators. It is probable that the immune response against the causative microorganism has an important role in the pathogenesis of Yerszwz'iz-triggered reactive arthritis. Yersinia antigens have been detected in synovial membrane and in synovial fluid cells in patients with reactive arthritis, and the longstanding antibody response may be a reflection of the continuous stimulation by the microbes hiding in, for example, gut-associated lymphoid tissues.
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