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Gene cloning of a novel cytokine inducing ICAM-1

诱导 ICAM-1 的新型细胞因子的基因克隆

基本信息

批准号：
04670382
负责人：
MIYASAKA Nobuyuki
金额：
$ 1.41万
依托单位：
Tokyo Medical and Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1994
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04670382/
关键词：
adhesion molecule matastasis vascular endothelial cells ICAM-1 VCAM-1 ELAM-1 サイトカイン

项目摘要

The interaction between lymphoma cells and vascular endothelial cells (EC) is the first critical step in the ivasion of lymphoma cells. We found that invasive human CCRF-CEM T lymphoma cells (CEM) released a factor that upregulates the expression of adhesion molecules on vascular EC.The supernatant of CEM (CEM-SUP) increased the expression of both ICAM-1 and ELAM-1 in time- and dose-dependent manners as shown by cell enzyme-linked immunoadsobent assay (ELISA). In contrast, the induction of VCAM-1 on EC with CEM-SUP was relatively weak. No reactivity for interleukin-lalpha, interleukin-1 beta, interferon-gamma, or tumor necrosis factor alpha, which are known to augment ICAM-1 expression, was detected in CEM-SUP by ELISA.In reverse transcriptase polymerase chain reaction (RT-PCR) assay, CEM expressed a minimum amount of tumor necrosis factor alpha mRNA but absolutely no interleukin 1 beta and interferon gamma mRNA.In addition, anttibodies to cytokines did not inhibit the upregulatory effect of CEM-SUP.Semipurified CEM-SUP further increased the cellular binding between CEM cells and EC in vitro. This factor was stabel to heat (65ﾟC,30 min) and labile to acid (pH2). Gel filtration and chromatofocusing estimated its molecular weight at 50 with an isoelectric point of ph 7.2. Produciton of this factor might contribute the invasive charcter of cEM through upregulation of adhesion molecules on EC.

淋巴瘤细胞与血管内皮细胞（vascular endothelial cells，EC）之间的相互作用是淋巴瘤细胞侵袭的第一个关键步骤。我们发现，侵袭性人CCRF-CEM T淋巴瘤细胞（CEM）释放一种因子，可上调血管内皮细胞表面粘附分子的表达，细胞酶联免疫吸附试验（ELISA）显示CEM上清（CEM-10）可上调ICAM-1和ELAM-1的表达，并呈时间和剂量依赖性。相反，VCAM-1对CEM-BMPs的EC的诱导作用相对较弱。ELISA法检测到CEM中没有白细胞介素-1 α、白细胞介素-1 β、干扰素-γ或肿瘤坏死因子α的反应性，而这些物质已知会增加ICAM-1的表达。在逆转录聚合酶链反应（RT-PCR）测定中，CEM表达最少量的肿瘤坏死因子α mRNA，但绝对没有白细胞介素-1 β和干扰素-γ mRNA。此外，细胞因子的拮抗剂不能抑制CEM-β 1的上调作用，半纯化的CEM-β 1能进一步增强CEM细胞与EC的体外结合。该因子对热（65 ℃，30 min）稳定，对酸（pH 2）不稳定。凝胶过滤和色谱聚焦估计其分子量为50，等电点为pH7.2。该因子的产生可能通过上调EC表面粘附分子的表达而促进cEM的侵袭性。