The Study of Antibody to Outer-Surface Protein A of Borrelia burgdorferi and Rheumatoid arthritis

碩士 === 中山醫學大學 === 免疫學研究所 === 93 === OBJECTIVE: Borrelia burgdorferi (Bb) is the causative agent of Lyme disease. In the chronic stage of Lyme disease, the Outer surface protein A (OspA) of Bb can trigger autoimmunity in the joint by molecular mimicry. IgG antibody responsed to OspA were found in abo...

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Bibliographic Details
Main Authors: Han-Wen, 劉瀚文
Other Authors: Gregory J. Tsay
Format: Others
Language:zh-TW
Published: 2005
Online Access:http://ndltd.ncl.edu.tw/handle/00054764429540472555
Description
Summary:碩士 === 中山醫學大學 === 免疫學研究所 === 93 === OBJECTIVE: Borrelia burgdorferi (Bb) is the causative agent of Lyme disease. In the chronic stage of Lyme disease, the Outer surface protein A (OspA) of Bb can trigger autoimmunity in the joint by molecular mimicry. IgG antibody responsed to OspA were found in about 70% of patients with Lyme arthritis. We use recombinant protein to detect anti-OspA antibody in patients with autoimmune disease (AID). The relationship between OspA antibody and patients with autoimmune disease were estimated in the study. METHODS: Recombinant antigens of OspA of Bb were tested with patients with AID in enzyme-linked immunosorbent assay (ELISA). The serum sample consisted of 68 patients with Rheumatoid arthritis (RA), Systemic lupus erythmatosus (SLE), Söjogren’s syndrome (SS), and 12 patients with Ankylosing spondylitis (AS). The 76 serums of health group were also obtained. RESULT: In analyses of anti-OspA IgG antibodies, 12(22%) of 68 patient serums with RA, 7(10%) of 68 patient serums with SEL, 6(8.8%) of 68 patient serums with SS and 3(25%) of patient serums with AS showed reactivity to OspA. In analyses of anti-OspA IgM antibodies, 20(29.4%) of 68 patient serums with RA, 8(11.8%) of patient serums with SLE, 8(11.8%) of patient serums with SS and 1(8.3%) of 12patient serums with AS, showe reactivity to OspA. In patient group of RA, the titer of anti-OspA IgG antibodies was significantly higher than normal group (p<0.05). The titer of anti-OspA IgM antibodies was more significant (p<0.001). The serologic tests for diagnosis of lyme disease have no response in all of the patients with anti-OspA antibodies CONCLUSION: This is first time that detect anti-OspA antibody in AID patients. Our result shows that the patients with RA were higher anti-OspA antibody and the most in AID patient. We suggest that the anti-OspA antibody was an autoantibody. The relationship between OspA antibody and rheumatoid arthritis should be estimated in the future.