The T helper cell response in Lyme arthritis: differential recognition of Borrelia burgdorferi outer surface protein A in patients with treatment-resistant or treatment-responsive Lyme arthritis.
Open Access
- 1 December 1994
- journal article
- clinical trial
- Published by Rockefeller University Press in The Journal of Experimental Medicine
- Vol. 180 (6), 2069-2078
- https://doi.org/10.1084/jem.180.6.2069
Abstract
The 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, approximately 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 B. burgdorferi is different in patients with treatment-responsive or treatment-resistant Lyme arthritis. For this purpose, 313 B. 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 treatment-resistant 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 treatment-resistant 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 B. burgdorferi OspA is involved in the pathogenesis of treatment-resistant Lyme arthritis.Keywords
This publication has 48 references indexed in Scilit:
- In vivo administration of interleukin‐2 turns on anergic self‐reactive T cells and leads to autoimmune diseaseEuropean Journal of Immunology, 1992
- The Clinical Evolution of Lyme ArthritisAnnals of Internal Medicine, 1987
- Molecular mimicry and autoimmune diseaseCell, 1987
- Failure of tetracycline therapy in early lyme diseaseArthritis & Rheumatism, 1987
- Antigens of Borrelia burgdorferi recognized during Lyme disease. Appearance of a new immunoglobulin M response and expansion of the immunoglobulin G response late in the illness.Journal of Clinical Investigation, 1986
- Proliferative responses of mononuclear cells in Lyme disease. Reactivity to Borrelia burgdorferi antigens is greater in joint fluid than in bloodArthritis & Rheumatism, 1986
- Lyme disease spirochetes induce human and murine interleukin 1 production.The Journal of Immunology, 1985
- Successful Parenteral Penicillin Therapy of Established Lyme ArthritisNew England Journal of Medicine, 1985
- Lyme Disease—a Tick-Borne Spirochetosis?Science, 1982
- Chronic Lyme ArthritisAnnals of Internal Medicine, 1979