| Summary: | 碩士 === 慈濟大學 === 微免暨分子醫學研究所 === 96 === The etiopathology of many autoimmune diseases is not well characterized. There are three factors involved in tolerance break, including environment, genetics and hormone. According to our studies, up to 86 ％ of local Systemic lupus erythematosus (SLE) patients have anti-HCMV(Humancytomegalovirus)-pp65 antibody. Partial mapping the associated B cell epitope in pp65 antigen found that only the pp65-3, that cover one third of the entire pp65 on the C terminal, was recognized by sera of SLE patients. We found that the anti-HCMV-pp65-3 antibody from previously immunized animals cross react to unknown proteins from Hela extract. Moreover, results further demonstrated that sera of SLE patients recognize HCMV-pp65 AA378-AA455 at a much higher frequency than other HCMV proteins. We hypothesize that a pathogenic B cell epitope whichinduce autoimmunity may locate in the pp65 AA422-AA439 region. In this proposal, we immunized BALB/c mice with either AA379-AA455 (N protein) or AA336-379 (H protein) in hope to induce autoantibody and possible clinical symptoms. From immunoblot, we found that both anti-HCMV-pp65 AA336-AA379 and anti HCMV-pp65-AA379-455 antibody form immunized mice cross react to unknown Hela proteins. Furthermore, kidneys of HCMV-pp65 AA336-AA379 immunized animals were positive for immune complex precipitation. We suggested that HCMV-pp65 AA336-AA379 may contain pathogenic epitope to lupus prone animals.
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