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异种移植新生儿心肌细胞的长期存活率通过腺病毒介导的CTLA4-Ig表达和CD40阻断.

Tao-Sheng Li¹, Hiroshi Ito, Koji Kajiwara

¹Division of Cardiovascular Surgery, Department of Medical Bioregulation, Yamaguchi University School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi, Japan 755-8505.

|September 25, 2003

概括

此摘要是机器生成的。

通过CTLA4-Ig基因转移和CD40阻断阻断CD28/B7共刺激途径,促进异种移植新生儿心肌细胞的长期存活. 这一策略增强了宿主心肌细胞的细胞融合和活力.

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科学领域:

免疫学免疫学免疫学
心脏病学心脏病学
再生医学是一种再生医学.

背景情况:

新生儿心肌细胞的外移植为心脏修复提供了潜在的机会.
免疫排斥限制了异种移植细胞的生存.
CD28/B7和CD40/CD40L共刺激途径在免疫反应中至关重要.

研究的目的:

评估异种移植新生儿心肌细胞的长期存活率.
调查CTLA4-Ig基因转移与CD40阻断相结合的疗效,以提高异种移植的存活率.

主要方法:

新生小鼠心肌细胞感染了表达CTLA4-Ig的腺病毒载体.
感染的心肌细胞被移植到C3H/He小鼠心肌中.
小鼠接受了抗CD40L单克隆抗体 (MR1) 或控制免疫球蛋白的腹腔内注射.
免疫组织化学被用来评估异种移植的存活率和整合.

主要成果:

腺病毒介导的CTLA4-Ig表达导致异种移植成功存活长达6个月.
暂时的CD40阻塞与MR1进一步支持异种移植的生存和整合.
在异种移植和宿主心肌细胞之间形成的间隙结.
没有免疫调节的对照组显示,异种移植存活时间超过2周是最小的.

结论:

腺病毒介导的CTLA4-Ig表达有效延长异种移植新生儿心肌细胞的存活时间.
暂时的CD40阻断补充CTLA4-Ig疗法,提高异种移植的长期活力.
这种综合免疫调节方法对基于细胞的心脏疗法具有前景.