Targeted disruption of CD43 gene enhances T lymphocyte adhesion.

Targeted disruption of CD43 gene enhances T lymphocyte adhesion.
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CD43 基因的靶向破坏可增强 T 淋巴细胞粘附。

DOI:
10.4049/jimmunol.151.3.1528
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发表时间:
1993
影响因子:
4.4
通讯作者:
B. Ardman
B. Ardman
中科院分区:
医学2区
文献类型:
--
作者:
N. Manjunath;Randall S. Johnson;Donald E. Staunton;Renata Pasqualini;B. Ardman

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CD 43是一种主要的白细胞表面糖蛋白,被认为对T淋巴细胞粘附和活化具有重要功能。我们通过基因打靶技术消除人T淋巴细胞系CEM中CD 43的表达,然后检测其粘附表型,来研究CD 43的功能。CEM细胞CD 43表达的丧失增强了它们与两种不同配体纤连蛋白和HIV-1 gp 120的同型粘附和结合。抗β 1整合素单克隆抗体特异性阻断了同型粘附的增强,抗β 1整合素单克隆抗体和抗CD 4单克隆抗体分别特异性阻断了与纤连蛋白和gp 120结合的增强。CD 43阴性细胞中CD 43表达的部分重建导致相应的逆转为粘附性较低的表型。这些数据表明,CD 43干扰T淋巴细胞粘附和CD 43可以调节淋巴细胞粘附,通过提供一个阈值,必须克服细胞-细胞和细胞-配体相互作用发生。
CD43 is a major leukocyte surface glycoprotein thought to have important functions for T lymphocyte adhesion and activation. We investigated the function of CD43 by using gene targeting to eliminate CD43 expression in the human T lymphocyte line CEM and then testing their adhesive phenotype. Loss of CD43 expression by the CEM cells enhanced their homotypic adhesion and binding to two distinct ligands, fibronectin and HIV-1 gp120. The enhanced homotypic adhesion was blocked specifically by an anti-beta 1 integrin mAb, and the enhanced binding to fibronectin and gp120 was blocked specifically by anti-beta 1 integrin and anti-CD4 mAb, respectively. Partial reconstitution of CD43 expression in the CD43-negative cells resulted in a corresponding reversion to a less adhesive phenotype. These data suggest that CD43 interferes with T lymphocyte adhesion and that CD43 can regulate lymphocyte adhesion by providing a threshold that must be overcome for cell-cell and cell-ligand interactions to occur.
DOI: 10.1073/pnas.86.4.1328
发表时间: 1989-02-01
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