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重症肌无力转基因小鼠模型的建立
  • 期刊名称:延边大学医学学报, 2006, 29(2): 79-81
  • 时间:0
  • 分类:R332[医药卫生—人体生理学;医药卫生—基础医学]
  • 作者机构:[1]延边大学基础医学院免疫学与病原生物学教研部,吉林延吉133000, [2]Department of Neurology, Faculty of Medicine,University of Maastricht, Maastricht, the Netherlands
  • 相关基金:国家自然科学基金(30460128)
  • 相关项目:特异性免疫吸附剂对家兔实验性重症肌无力的治疗
中文摘要:

[目的]建立人免疫球蛋白转基因小鼠实验性自身免疫性重症肌无力模型.[方法]用电鳐电器官分离纯化的乙酰胆碱受体免疫人免疫球蛋白转基因小鼠,以肌肉收缩力判定病情,以放射免疫测定法测定动物血清中抗乙酰胆碱受体抗体滴度及动物全身肌肉乙酰胆碱受体浓度.[结果]实验动物血清中抗乙酰胆碱受体抗体滴度为6~296nmol,全身肌肉乙酰胆碱受体损失率最高达65%,部分动物出现肌肉收缩无力表现.[结论]成功地建立了人免疫球蛋白转基因小鼠实验性自身免疫性重症肌无力模型.

英文摘要:

OBJECTIVE To set up a new model of experimental autoimmune myasthenia gravis (EAMG) in mice transgenic for human immunoglobulin (Ig) loci. METHODS Mice transgenic for human Ig were immunized with acetylcholine receptor (AChR), isolated and purified from electronic organs of Torpedo. The severity of clinical signs of disease was scored by measuring muscular weakness. The anti-Torpedo AChR antibody titer, and the concentration of AChR in muscle were determined by radioimmunoassay. RESULTS The titers of anti-Torpedo AChR antibodies in sera ranged from 6 to 296 nmol. The AChR loss in the muscle of Torpedo AChR-immunized mice was up to 65% compared to control mice. Furthermore, the muscular weakness was induced in some of the mice CONCLUSION A model of EAMG was successfully induced in mice transgenic for human Ig.

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