Abstract
The contribution of certain Gram-negative bacteria and host HLA class I Ag to the development of reactive arthritis (ReA)3 has strong epidemiologic support but the pathogenesis of the arthritis is unknown. An outbreak of Salmonella typhimurium afforded the opportunity to compare the immune response to the organism between those who developed ReA (ReA+, n = 11) with those who did not (ReA-, n = 12). Of the 11 ReA+ patients, 4 were B27-positive and 6 were B7-positive; of the ReA- patients none was B27- or B7-positive. The causative pathogen S. typhimurium phage 22 was used to examine PBL proliferation by [3H]thymidine incorporation. Impairment in lymphocyte response to S. typhimurium in ReA+ compared with ReA- was demonstrated by: i) lower stimulation index (1.9 +/- 0.3 for ReA+, 5.7 +/- 0.6 for ReA-, p less than 0.01); ii) lower in vitro Ig production; and iii) lower Ag-induced IL-2 production. Mixing experiments did not demonstrate a soluble suppressor factor in ReA+ supernatants. Thus, after infection with S. typhimurium there is an impairment in cellular immunity that has correlates in immunogenetic and clinical features of the infected population.
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