Correction of CD18-deficient lymphocytes by retrovirus-mediated gene transfer.
Correction of CD18-deficient lymphocytes by retrovirus-mediated gene transfer.
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通过逆转录病毒介导的基因转移纠正 CD18 缺陷淋巴细胞。
DOI：
10.1126/science.1972597
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Todd,RF
中科院分区：
文献类型：
--
作者：
Wilson,JM;Ping,AJ;Krauss,JC;Mayo-Bond,L;Rogers,CE;Anderson,DC;Todd,RF
白细胞粘附缺陷（LAD）是一种由CD18表达紊乱引起的遗传性白细胞功能紊乱。通过逆转录病毒介导的功能性CD18基因转导，一名LAD患者淋巴细胞系的遗传和功能异常得到了纠正。将LAD患者的淋巴细胞暴露于表达CD18的逆转录病毒中，并富集细胞表面表达CD11a和CD18 （LFA-1）的细胞。这些细胞的分子和功能分析显示：(i)每个细胞有一个前病毒序列的拷贝，（ii）病毒导向的CD18 RNA超过正常的内源性水平，（iii）细胞表面CD11a和CD18蛋白的正常数量，以及（iv） lfa -1依赖性粘附功能的重建。
Leukocyte adhesion deficiency (LAD) is an inherited disorder of leukocyte function caused by derangements in CD18 expression. The genetic and functional abnormalities in a lymphocyte cell line from a patient with LAD have been corrected by retrovirus-mediated transduction of a functional CD18 gene. Lymphocytes from patients with LAD were exposed to CD18-expressing retrovirus and enriched for cells that express CD11a and CD18 (LFA-1) on the cell surface. Molecular and functional analyses of these cells revealed (i) one copy of proviral sequence per cell, (ii) viral-directed CD18 RNA that exceeded normal endogenous levels, (iii) normal quantities of CD11a and CD18 protein on the cell surface, and (iv) reconstitution of LFA-1-dependent adhesive function.