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[一种新的共刺激分子——B7 同源物 6 的研究进展——综述]

[Research Advances of A New Co-stimulatory Molecule-B7 Homolog 6--Review].

作者信息

Wu Fei-Fei, Ke Xiao-Yan

机构信息

Department of Hematology, Peking University Third Hospital, Beijing 100191, China.

Department of Hematology, Peking University Third Hospital, Beijing 100191, China. E-mail:

出版信息

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2016 Feb;24(1):295-8. doi: 10.7534/j.issn.1009-2137.2016.01.057.

Abstract

B7-H6 is a co-stimulatory molecule discoveried recently. B7-H6 is not expressed on normal cells, but specially expressed on tumor cells. It can also be expressed on antigen presenting cells (APC) by the induction. The B7-H6 expression can be downregulated by HDACi. NK cells can be activated to release TNFα and IFNγ through B7H6-NKp30 pathway. The B7-H6 molecules expressed on the cell surface can be shedded to form soluble molecules. In the meantime, the B7-H6/NKp30 pathway may be involved in the pathogenesis of primary Sjogren syndrome. B7-H6/NKp30 may become a new therapeutic target for tumor, inflammation and autoimmune diseases. This review discusses the B7-H6 and receptor sructure, the expression and significance of B7-H6, the function and regulating mechanism of B7-H6 and the soluble molecules of B7-H6.

摘要

B7-H6是一种最近发现的共刺激分子。B7-H6在正常细胞上不表达,但在肿瘤细胞上特异性表达。它也可通过诱导在抗原呈递细胞(APC)上表达。B7-H6的表达可被组蛋白去乙酰化酶抑制剂(HDACi)下调。自然杀伤(NK)细胞可通过B7H6-NKp30途径被激活以释放肿瘤坏死因子α(TNFα)和干扰素γ(IFNγ)。细胞表面表达的B7-H6分子可脱落形成可溶性分子。同时,B7-H6/NKp30途径可能参与原发性干燥综合征的发病机制。B7-H6/NKp30可能成为肿瘤、炎症和自身免疫性疾病的新治疗靶点。本文综述讨论了B7-H6及其受体结构、B7-H6的表达及意义、B7-H6的功能及调控机制以及B7-H6的可溶性分子。

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