Intercellular cell adhesion molecule-1,vascular cell adhesion molecule-1, and regulated on activation normal T cell expressed and secreted are expressed by human breast carcinoma cells and support eosinophil adhesion and activation
Intercellular cell adhesion molecule-1,vascular cell adhesion molecule-1, and regulated on activation normal T cell expressed and secreted are expressed by human breast carcinoma cells and support eosinophil adhesion and activation
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DOI：
10.1016/s0002-9440(10)64542-7
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发表时间：
2000-07-01
影响因子：
6
通讯作者：
Patel, KD
中科院分区：
文献类型：
--
作者：
Ali, S;Kaur, J;Patel, KD
嗜酸性粒细胞通常与寄生虫病和过敏性疾病有关;然而，嗜酸性粒细胞增多症也在几种类型的人类肿瘤中观察到，包括乳腺癌。在这项研究中，我们研究了几种人乳腺癌细胞系的粘附分子表达和结合和激活嗜酸性粒细胞的能力，MDA-MB-435 S和MDA-MB-468细胞组成性表达细胞间粘附分子-1（ICAM-1）和血管细胞粘附分子-1（VCAM-1），这种表达通过肿瘤坏死因子-α（TNF-α）处理而增强。BT-20和SK-BR-3细胞在TNF-α刺激后仅表达ICAM-1或VCAM-1。嗜酸性粒细胞与MDA-MB-435 S细胞组成性结合，但不与BT-20细胞结合。用TNF-γ刺激可轻微增强嗜酸性粒细胞对MDA-MB-435 S细胞的粘附，并显著增加对BT-20细胞的粘附。用抗α 4-整联蛋白单克隆抗体阻断了嗜酸性粒细胞与这些细胞系的粘附。两种MDA-MB-435 S酸性BT-20细胞也释放嗜酸性粒细胞活化剂。TNF-α处理的细胞系上清液增加了嗜酸性粒细胞与纤连蛋白的粘附，并增加了嗜酸性粒细胞穿过纤连蛋白包被的transwell板的迁移。酶联免疫吸附试验表明，TNF-α刺激的乳腺癌细胞释放的趋化因子调节活化，T细胞表达和分泌（RANTES）。向乳腺癌细胞上清液中添加抗RANTES抗体部分阻断了嗜酸性粒细胞的激活，表明这些上清液中的RANTES参与了嗜酸性粒细胞的激活。这些数据表明，TNF-α刺激的乳腺癌细胞表达可以结合和激活嗜酸性粒细胞的介质，这表明嗜酸性粒细胞定位于乳腺癌部位的机制。
Eosinophils are usually associated with parasitic and allergic diseases; however, eosinophilia is also observed in several types of human tumors, including breast carcinomas. In this study we examined several human breast carcinoma cell lines for adhesion molecule expression and the ability to bind and activate eosinophils, MDA-MB-435S and MDA-MB-468 cells constitutively expressed both intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and this expression was enhanced by treatment with tumor necrosis factor-alpha (TNF-alpha). BT-20 and SK-BR-3 cells only expressed ICAM-1 or VCAM-1 after stimulation with TNF-alpha. Eosinophils constitutively bound to MDA-MB-435S cells, but not to BT-20 cells. Stimulation with TNF-ly slightly enhanced eosinophil adhesion to MDA-MB-435S cells and dramatically Increased adhesion to BT-20 cells. Greater than 80% of eosinophil adhesion to these cell lines was blocked with an anti-alpha 4-integrin monoclonal antibody. Both MDA-MB-435S acid BT-20 cells also released eosinophil activator(s), Supernatants from TNF-alpha-treated, but not control-treated, cell lines increased eosinophil adhesion to fibronectin and increased eosinophil transmigration across fibronectincoated transwell plates. Enzyme-Linked immunosorbent assays showed that TNF-alpha-stimulated breast carcinoma cells released the chemokine regulated on activation, T cell expressed and secreted (RANTES). Addition of an anti-RANTES antibody to breast carcinoma cell supernatants partially blocked eosinophil activation suggesting that RANTES in these supernatants was participating In eosinophil activation These data show that TNF-alpha-stimulated breast carcinoma cells express mediators that can both bind and activate eosinophils, suggesting a mechanism for eosinophil localization to breast carcinoma sites.