Human T-Cell Leukemia Virus Type I Tax Protein Induces the Expression of IL-6R and soluble IL-6R production
人 T 细胞白血病病毒 I 型 Tax 蛋白诱导 IL-6R 表达和可溶性 IL-6R 产生
基本信息
- 批准号:12670275
- 负责人:
- 金额:$ 1.22万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2000
- 资助国家:日本
- 起止时间:2000 至 2001
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Aim : The soluble interleukin 6 receptor (sIL-6R) circulates at elevated levels in HTLV-I infected patients compared with the healthy person. To elucidate the cause of this high level release of SIL-6R in HTLV-I infected patients, we investigated expression of the IL-6R or sIL-6R in T-cells infected with HTLV-I. Results and DiscussionrThrough our examination, it was found that although some HTLV-I-non infected cell lines expressed IL-6R, all HTLV-I-infected cell lines tested expressed IL-6R.Results and Discussion : Through our examination, it was found that although some HTLV-I-non-infected cell lines expressed IL-6R, all HTLV-I-infected cell lines tested expressed IL-6R, Although the TY8-3 T-cell established from a thymoma did not express IL-6R, the HTLV-I infected isogenic cell lines, TY8-3/MT-2 and TY8-3/TCL-Kan expressed IL-6R. The release of proteolytically cleaved (PC)-sIL-6R was demonstrated on MT-2, MT-4, TY8-3/MT-2 and TY8 3/TCL-Kan, but not HTLV-I negative parental TY8-3 by ELISA. Induction of the Tax in JPX-9 cells by CdCl_2 results in the expression of not only IL-6R but also release of the PC-IL-6R, but not in JPX-9/M. Our results demonstrate that expression of the IL-6R and release of the PC-'sIL 6R are induced by HTLV-I or Tax. Hence, it may contribute to affected tissues, in HTLV-I associated inflammatory diseases, because the presence of sIL-6R is central to the regulation of IL-6-mediated responses in signaling for inflammatory cytokine IL-6 in the cells which are not expressed the cognate IL-6R.
目的:与健康人相比,HTLV-1感染患者的可溶性白介素6受体(SIL-6R)在升高的水平下循环。为了阐明在HTLV-I感染患者中SIL-6R的高水平释放的原因,我们研究了感染HTLV-I的T细胞中IL-6R或SIL-6R的表达。结果和讨论通过我们的检查,发现尽管某些HTLV-I-non感染的细胞系表示IL-6R,但所有HTLV-I感染的细胞系测试均表达IL-6R. Results和讨论:通过我们的检查:发现它,发现尽管某些HTLV-I未感染的细胞系表示IL-6R,但所有htlv-i感染的细胞系都测试了表达IL-6R的细胞系,尽管从胸腺瘤建立的TY8-3 T细胞均未表达IL-6R,但HTLV-I感染的ISEGENIC细胞系TY8-3/MT-2和TY8-3/TCL-KAN表达IL-6R。 ELISA在MT-2,MT-4,TY8-3/MT-2和TY8 3/TCL-KAN上释放(PC)-SIL-6R在MT-2,MT-4,TY8-3/MT-2和TY8 3/TCL-KAN上证明了ELISA的HTLV-I负亲属TY8-3 。通过CDCL_2在JPX-9细胞中诱导税收不仅会导致IL-6R的表达,还会释放PC-IL-6R,而在JPX-9/m中则释放。我们的结果表明,IL-6R的表达和PC-'SIL 6R的释放是由HTLV-I或税收诱导的。因此,在HTLV-I相关炎性疾病中,它可能有助于受影响的组织,因为SIL-6R的存在对于不属于不属于的炎性细胞因子IL-6的信号传导调节IL-6介导的反应至关重要。表示同源IL-6R。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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HORIUCHI Sankichi其他文献
HORIUCHI Sankichi的其他文献
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{{ truncateString('HORIUCHI Sankichi', 18)}}的其他基金
Plasmids and pathogenicity of Salmonella braenderup and Salmonella typhimurium
布伦德鲁普沙门氏菌和鼠伤寒沙门氏菌的质粒和致病性
- 批准号:
61570204 - 财政年份:1986
- 资助金额:
$ 1.22万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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