PubMed · 1989 · 123 citations · 26 references
Life SciencesImmunologyPathologyAutoimmunityInflammationRheumatologyAntigen RecognitionCell-mediated ImmunityImmune Responses To InfectionInflammatory ArthritisJoint DiseaseSynovial InflammationImmune-mediated ArthritisMhc Class Ii MoleculesPeripheral ArthritisPost-infectious ArthritisT Cell Responses To Bacterial InfectionT Cell-mediated Immune ResponseT-cell Mediated Immune ResponseT-cell Mediated Responses
Reactive arthritis (ReA) is believed to be "triggered' by infection with certain bacteria. When the proliferative responses of mononuclear cells (MC) obtained from the synovial fluid (SF) of ReA patients were examined, it was found that they responded maximally to the specific organism responsible for the preceding infection. The response was shown to be due to Class II MHC-restricted T cells by inhibition experiments using cyclosporin A and monoclonal antibodies. Significant SFMC responses to additional organisms associated with ReA were also recorded; since there was no serological evidence of preceding infection by these organisms, this finding suggests that these bacteria share common T cell-recognized antigenic epitopes. The corresponding responses by peripheral blood mononuclear cells (PBMC) were much lower and often barely detectable, whereas their responses to PHA were consistently higher than those of SFMC. These results, combined with evidence that bacterial antigens localize in the joint, indicate that a bacteria-specific, T-cell-mediated response may play a central role in the pathogenesis of ReA.
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revision of diagnostic criteria for rheumatoid arthritis
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Loss of CD45R and gain of UCHL1 reactivity is a feature of primed T cells.
Arne N. Akbar, Linda A. Terry, Anthony Timms et al. · The Journal of Immunology · 1988 · 925 citations · Full text
Yersinia Antigens in Synovial-Fluid Cells from Patients with Reactive Arthritis
Kaisa Granfors, Sirpa Jalkanen, R. von Essen et al. · New England Journal of Medicine · 1989 · 481 citations
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