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抑瘤素M刺激人肝癌HepG2细胞中白细胞介素-6受体的表达和释放。

Oncostatin M stimulates the expression and release of the IL-6 receptor in human hepatoma HepG2 cells.

作者信息

Cichy J, Rose-John S, Potempa J, Pryjma J, Travis J

机构信息

Department of Microbiology and Immunology, Institute of Molecular Biology, Jagiellonian University, Krakow, Poland.

出版信息

J Immunol. 1997 Dec 1;159(11):5648-53.

PMID:9548508
Abstract

Soluble IL-6R (sIL-6R), which lacks the transmembrane domain, has been suggested to be a potent immunomodulator of IL-6 biologic activity. In this study, the ability of cells of hepatic origin to generate the sIL-6R was investigated. It was found that oncostatin M alone or in combination with the glucocorticoid analogue dexamethasone significantly up-regulated IL-6R release. Oncostatin M appeared to generate the sIL-6R primarily through an alternative splicing mechanism. Since sIL-6R is able to form biologically active complexes with IL-6, the release of the sIL-6R from hepatocytes may be important to sensitize cells lacking the membrane-bound receptor, particularly during an acute phase reaction.

摘要

可溶性白细胞介素-6受体(sIL-6R)缺乏跨膜结构域,被认为是白细胞介素-6生物活性的一种强效免疫调节剂。在本研究中,对肝源性细胞产生sIL-6R的能力进行了研究。发现单独使用抑瘤素M或与糖皮质激素类似物地塞米松联合使用时,可显著上调白细胞介素-6受体的释放。抑瘤素M似乎主要通过一种可变剪接机制产生sIL-6R。由于sIL-6R能够与白细胞介素-6形成生物活性复合物,肝细胞释放sIL-6R对于使缺乏膜结合受体的细胞敏感化可能很重要,尤其是在急性期反应期间。

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