Nambu M, Mayumi M, Mikawa H
Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
Cell Immunol. 1992 Sep;143(2):335-47. doi: 10.1016/0008-8749(92)90030-s.
The effects of several cytokines and phorbol myristate acetate (PMA) on LFA-1 and ICAM-1 expression on a human eosinophilic leukemia cell line, EoL-3, were investigated and compared with those of a human monocytic leukemia cell line, U937. EoL-3 cells expressed large amounts of LFA-1 and small amounts of ICAM-1, and their expression was regulated similarly in EoL-3 cells and U937 cells. Interferon-gamma (IFN-gamma) enhanced ICAM-1 expression but not LFA-1 expression, and PMA augmented both LFA-1 and ICAM-1 expression. IFN-gamma and PMA showed an additive effect on ICAM-1 expression. These results collectively suggest that expression of LFA-1 and ICAM-1 is regulated differently and that IFN-gamma and PMA regulate the expression through different mechanisms. PMA but not IFN-gamma induced homotypic adhesion of EoL-3 and U937 cells, suggesting that PMA but not IFN-gamma activated the adhesive function of these cells. Staurosporin, an inhibitor of protein kinases (PKs), partly suppressed IFN-gamma- and PMA-augmented expression of ICAM-1 on EoL-3 and U937 cells, but did not affect PMA-augmented LFA-1 expression, suggesting that staurosporin-sensitive PKs are involved in IFN-gamma- and PMA-augmented ICAM-1 expression but not in PMA-augmented LFA-1 expression. The role of protein kinase C (PK-C) in these mechanisms was not revealed because a PK-C inhibitor, H-7, did not show any definitive effect on IFN-gamma- and PMA-induced expression of LFA-1 and ICAM-1. Moreover, cyclic AMP (cAMP)- and cGMP-dependent pathways were not shown to be involved in the augmentation of the expression of these molecules.
研究了几种细胞因子和佛波酯（PMA）对人嗜酸性粒细胞白血病细胞系EoL-3上淋巴细胞功能相关抗原-1（LFA-1）和细胞间黏附分子-1（ICAM-1）表达的影响，并与人类单核细胞白血病细胞系U937进行了比较。EoL-3细胞表达大量的LFA-1和少量的ICAM-1，其表达在EoL-3细胞和U937细胞中受到类似的调节。γ干扰素（IFN-γ）增强ICAM-1表达但不增强LFA-1表达，而PMA增加LFA-1和ICAM-1的表达。IFN-γ和PMA对ICAM-1表达显示出相加效应。这些结果共同表明，LFA-1和ICAM-1的表达受到不同的调节，并且IFN-γ和PMA通过不同的机制调节表达。PMA而非IFN-γ诱导EoL-3和U937细胞的同型黏附，表明PMA而非IFN-γ激活了这些细胞的黏附功能。蛋白激酶（PK）抑制剂星形孢菌素部分抑制IFN-γ和PMA增强的EoL-3和U937细胞上ICAM-1的表达，但不影响PMA增强的LFA-1表达，表明星形孢菌素敏感的PK参与IFN-γ和PMA增强的ICAM-1表达，但不参与PMA增强的LFA-1表达。由于PK-C抑制剂H-7对IFN-γ和PMA诱导的LFA-1和ICAM-1表达未显示任何明确作用，因此未揭示蛋白激酶C（PK-C）在这些机制中的作用。此外，环磷酸腺苷（cAMP）和环磷酸鸟苷（cGMP）依赖性途径未显示参与这些分子表达的增强。
