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背景:目前Fas和Bcl-2基因在重症肌无力发病机制中的作用越来越受到重视,国内外已做了较多的研究,阐明调控Fas和Bcl-2基因的表达对重症肌无力发生及其疾病过程中的治疗均具有密切的关系。资料来源:应用计算机检索Medline数据库1990-01/2004-12期间的相关文献,检索词为“Fas”,“Bcl-2”,“MyastheniaGravis”及“gene”分别组合进行检索,限定文章语言种类为English。资料选择:对资料进行初审,选取包括上述Fas和Bcl-2与重症肌无力的文献,以及有关Fas和Bcl-2基因及基因治疗方面的文献,并且查找全文。资料提炼:搜集到大量介绍Fas和Bcl-2基因的文献,21篇有关Fas和Bcl-2与重症肌无力的文献以及32篇重症肌无力有关基因治疗方面的文献,选取有代表性的20篇文章纳入分析。资料综合:20篇文献中有8篇关于Fas基因及重症肌无力,5篇关于Bcl-2基因及重症肌无力,7篇关于基因手段治疗重症肌无力及免疫性疾病。结论:Fas和Bcl-2基因调节异常、表达失控与T淋巴细胞、胸腺细胞凋亡缺陷密切相关,与重症肌无力发病密切相关,从基因水平揭示重症肌无力的发病机制在基因水平诱导细胞凋亡以抑制自身抗体产生,将为重症肌无力的治疗提供新的手段。
BACKGROUND: At present, the role of Fas and Bcl-2 gene in the pathogenesis of myasthenia gravis has drawn more and more attention. More studies have been done both at home and abroad to elucidate the roles of Fas and Bcl-2 gene in the pathogenesis of myasthenia gravis and The course of disease treatment are closely related. DATA SOURCES: A computer-based online search of the Medline database was conducted between January 1990 and December 2004 with the search terms of “Fas”, “Bcl-2”, “Myasthenia Gravis” and “gene”, respectively. English. Data Selection: The data were reviewed first, and the literature including the above-mentioned Fas and Bcl-2 and myasthenia gravis, as well as the literature on Fas and Bcl-2 gene and gene therapy, were searched and the full text was searched. Data Extraction: A large number of literatures about Fas and Bcl-2 genes were collected, 21 articles on Fas and Bcl-2 and myasthenia gravis and 32 articles on gene therapy related to myasthenia gravis were selected. A representative 20 articles Articles included in the analysis. DATA SYNTHESIS: Eight articles in 20 articles on Fas gene and myasthenia gravis, 5 on Bcl-2 gene and myasthenia gravis, and 7 on gene therapy for myasthenia gravis and autoimmune diseases. CONCLUSIONS: Fas and Bcl-2 genes are abnormally regulated. The out-of-control expression of Fas and Bcl-2 genes is closely related to the apoptosis of T lymphocytes and thymocytes. It is closely related to the pathogenesis of myasthenia gravis. The pathogenesis of myasthenia gravis from the gene level induces apoptosis at the gene level Death to inhibit the production of autoantibodies, will provide a new means for the treatment of myasthenia gravis.