SummaryThe host response to Borrelia burgdorferi is likely to play a role in the pathogenesis of Lyme arthritis.Whereas most patients with Lyme arthritis can be cured with antibiotic therapy, ~10% of the patients have persistent arthritis for months or even several years after antibiotic treatment. In this study, we tested the hypothesis that the T cell response to one or more antigens of/~ burgdo~ri is different in patients with treatment-responsive or treatment-resistant Lyme arthritis. For this purpose, 313/~ burgdorferi-specific T cell lines were derived from the synovial fluid or peripheral blood of four patients with treatment-responsive Lyme arthritis and five patients with treatmentresistant arthritis. 87 T cell lines from treatment-responsive Lyme arthritis and 112 lines from the treatment-resistant group were examined for the recognition of five recombinant. B. burgdorferi proteins: outer surface proteins A (OspA), B, C, p39, and p93. In both groups of patients, the T cell lines frequently recognized OspB, and only occasionally recognized OspC, p39, and p93. In contrast, OspA was preferentially recognized by T cell lines from patients with treatmentresistant arthritis, but only rarely recognized by T cell lines from patients with treatment-responsive arthritis (odds ratio 28.4, 95% confidence interval 9.2-87.8, p <0.005). These results are compatible with the hypothesis that the T cell response to/~ burgdorferi OspA is involved in the pathogenesis of treatment-resistant Lyme arthritis."[me borreliosis, a tick-borne infection caused by the spirochete Borrelia burgdorferi, is a multisystem disorder.

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