A2 Refereed review article in a scientific journal
Pathogenesis of Yersinia-triggered reactive arthritis: immunological, microbiological and clinical aspects
Authors: Toivanen A, Granfors K, Lahesmaa-Rantala R, Leino R, Ståhlberg T, Vuento R
Publication year: 1985
Journal: Immunological Reviews
Journal name in source: Immunological reviews
Journal acronym: Immunol Rev
Volume: 86
First page : 47
Last page: 70
Number of pages: 24
ISSN: 0105-2896
DOI: https://doi.org/10.1111/j.1600-065X.1985.tb01137.x
Abstract
When a patient develops reactive arthritis after Yersinia enteritis, the following conditions are often fulfilled: the patient is HLA-B27-positive; however, some B27-negative individuals develop severe arthritis and some positives do not, in the initial phase, the diarrhea is milder, the anti-Yersinia antibody response of IgG class is more vigorous and persists longer, the anti-Yersinia antibody response of IgA class is more vigorous and persists much longer, the anti-Yersinia antibodies of IgA1 and IgA2 subclass, those with J-chain and, especially, those with secretory piece are produced more vigorously, indicating local immunostimulation close to the intestinal epithelium, in the early phase, Yersinia-IgM immune complexes are found in the circulation, and the lymphocyte transformation response against not only Yersinia but also against other gram-negative enteric bacteria is weaker. When all these aspects are considered together a strong suspicion arises that the patients who are destined to develop reactive arthritis fail in their first line of defense against the invading organism when contracting a Yersinia enteritis. This may lead to persistence of the microorganism within the body, e.g., in the intestinal epithelium or in the mesenteric lymphoid tissues, maintaining a stimulus for a prolonged--apparently futile and perhaps harmful--antibody production. Finally, the initiating and decisive factor should not be forgotten: the Yersinia. Why and how it triggers the process is at present one of the enigmas of the pathogenesis of reactive arthritis.
When a patient develops reactive arthritis after Yersinia enteritis, the following conditions are often fulfilled: the patient is HLA-B27-positive; however, some B27-negative individuals develop severe arthritis and some positives do not, in the initial phase, the diarrhea is milder, the anti-Yersinia antibody response of IgG class is more vigorous and persists longer, the anti-Yersinia antibody response of IgA class is more vigorous and persists much longer, the anti-Yersinia antibodies of IgA1 and IgA2 subclass, those with J-chain and, especially, those with secretory piece are produced more vigorously, indicating local immunostimulation close to the intestinal epithelium, in the early phase, Yersinia-IgM immune complexes are found in the circulation, and the lymphocyte transformation response against not only Yersinia but also against other gram-negative enteric bacteria is weaker. When all these aspects are considered together a strong suspicion arises that the patients who are destined to develop reactive arthritis fail in their first line of defense against the invading organism when contracting a Yersinia enteritis. This may lead to persistence of the microorganism within the body, e.g., in the intestinal epithelium or in the mesenteric lymphoid tissues, maintaining a stimulus for a prolonged--apparently futile and perhaps harmful--antibody production. Finally, the initiating and decisive factor should not be forgotten: the Yersinia. Why and how it triggers the process is at present one of the enigmas of the pathogenesis of reactive arthritis.