Perforin knockout mice, but not mice with MAIDS, show protection against experimental cytomegalovirus retinitis after adoptive transfer of immune cells with a functional perforin cytotoxic pathway
Perforin knockout mice, but not mice with MAIDS, show protection against experimental cytomegalovirus retinitis after adoptive transfer of immune cells with a functional perforin cytotoxic pathway
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DOI：
10.1007/s00705-004-0370-3
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发表时间：
2004-11-01
影响因子：
2.7
通讯作者：
Cousins, SW
中科院分区：
文献类型：
--
作者：
Dix, RD;Ekworomadu, CO;Cousins, SW
进行连续转移研究以检验穿孔素细胞毒性途径在保护免受实验性鼠巨细胞病毒（MCMV）视网膜炎方面比Fas/FasL细胞毒性途径更重要的假设。供体MCMV免疫的正常小鼠或Fas/FasL介导的细胞毒性缺陷的gld小鼠的脾免疫细胞在转移到穿孔素介导的细胞毒性缺陷的受体PKO小鼠中时，显著降低视网膜下MCMV攻击后MCMV视网膜炎的频率和严重程度。与此形成鲜明对比的是，供体MCMV免疫的PKO小鼠的脾细胞在转移到受体PKO小鼠时未能提供针对MCMV视网膜炎的保护。然而，在逆转录病毒诱导的免疫缺陷（MAIDS）的受体小鼠中，即使脾细胞来自MCMV免疫的正常小鼠，也没有达到保护作用。
Adoptive transfer studies were performed to test the hypothesis that the perforin cytotoxic pathway is more important than the Fas/FasL cytotoxic pathway in protection against experimental murine cytomegalovirus (MCMV) retinitis. Splenic immune cells from donor MCMV-immunized normal mice or gld mice deficient in Fas/FasL-mediated cytotoxicity significantly reduced the frequency and severity of MCMV retinitis following subretinal MCMV challenge when transferred into recipient PKO mice deficient in perforin-mediated cytotoxicity. In sharp contrast, splenic cells from donor MCMV-immunized PKO mice failed to provide protection against MCMV retinitis when transferred into recipient PKO mice. Protection was not achieved, however, in recipient mice with retrovirus-induced immunodeficiency (MAIDS), even when splenic cells originated from MCMV-immunized normal mice.