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Clinical and Vaccine Immunology, November 2007, p. 1437-1441, Vol. 14, No. 11
1071-412X/07/$08.00+0 doi:10.1128/CVI.00151-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Institute of Immunology,1 Department of Medicine, Chung Shan Medical University, Taichung, Taiwan,2 Department of Parasitology and Tropical Medicine, National Defense Medical Center, Taipei, Taiwan,3 Department of Pediatrics, University of Connecticut School of Medicine, Farmington, Connecticut4
Received 10 April 2007/ Returned for modification 5 July 2007/ Accepted 6 September 2007
Lyme arthritis and rheumatoid arthritis share common clinical features and synovial histology. It is unclear whether they also share similar pathogenesis. Previous studies have shown that the severity and duration of Lyme arthritis correlate directly with serum concentrations of antibody against outer surface protein A (OspA) of the causative pathogen Borrelia burgdorferi. We tested the sera of 68 subjects with rheumatoid arthritis, 147 subjects with other autoimmune diseases, and 44 healthy subjects who had never had Lyme disease, as well as sera of 16 patients who had Lyme disease, for reactivity against the B. burgdorferi OspA protein. The sera of about a quarter of the rheumatoid arthritis patients and a 10th of the autoimmune disease and Lyme disease patients reacted against OspA antigen. Of 50 rheumatoid arthritis patients who could be evaluated for disease severity, a 28-joint count disease activity score of >2.6 was noted for 11 of 15 (73%) patients whose sera reacted against OspA antigen and 13 of 35 (37%; P < 0.05) whose sera were nonreactive. Serum reactivity against OspA antigen is associated with the pathogenesis of rheumatoid arthritis.
Published ahead of print on 19 September 2007.
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