Coexpression of CD58 or CD48 with intercellular adhesion molecule 1 on target cells enhances adhesion of resting NK cells
Coexpression of CD58 or CD48 with intercellular adhesion molecule 1 on target cells enhances adhesion of resting NK cells
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DOI：
10.4049/jimmunol.170.1.294
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发表时间：
2003-01-01
影响因子：
4.4
通讯作者：
Long, EO
中科院分区：
文献类型：
--
作者：
Barber, DF;Long, EO
β(2) 整合素 LFA-1 (CD11a/CD18) 介导淋巴细胞与表达 ICAM 的细胞的粘附。这种粘附的强度受到细胞因子和趋化因子传递的不同信号的调节，在 T 细胞的情况下还受到 TCR 的调节。为了确定静息 NK 细胞粘附所需的受体-配体相互作用，产生了表达人类 NK 细胞受体配体不同组合的果蝇细胞。 ICAM-1 的单独表达足以粘附对 src 家族激酶和磷脂酰肌醇 3-激酶抑制剂敏感的静息 NK 细胞。静息 NK 细胞与固相 ICAM-1 的结合显示出类似的信号传导要求。 IL-2 或 IL-15 对静息 NK 细胞的脉冲导致对单独表达 ICAM-1 的昆虫细胞的肌动蛋白依赖性粘附强烈增强。 LFA-3 (CD58) 或 CD48 与 ICAM-1 的共表达导致静息 NK 细胞的强烈粘附，即使在没有细胞因子的情况下也是如此。因此，静息 NK 细胞上的 LFA-3 和 CD48 受体增强了 LFA-1 介导的粘附。
The beta(2) integrin LFA-1 (CD11a/CD18) mediates adhesion of lymphocytes to cells expressing ICAM. The strength of this adhesion is regulated by different signals delivered by cytokines and chemokines, and by the TCR in the case of T cells. To determine the receptor-ligand interactions required for adhesion of resting NK cells, Drosophila cells expressing different combinations of ligands of human NK cell receptors were generated. Expression of ICAM-1 alone was sufficient for an adhesion of resting NK cells that was sensitive to inhibitors of src family kinase and of phosphatidylinositol 3-kinase. Binding of resting NK cells to solid-phase ICAM-1 showed similar signaling requirements. A pulse of either IL-2 or IL-15 to resting NK cells resulted in strongly enhanced, actin-dependent adhesion to insect cells expressing ICAM-1 alone. Coexpression of either LFA-3 (CD58) or CD48 with ICAM-1 resulted in strong adhesion by resting NK cells, even in the absence of cytokines. Therefore, receptors for LFA-3 and CD48 on resting NK cells strengthen the adhesion mediated by LFA-1.