| 1 | Hypoxia induces T-cell apoptosis by inhibiting chemokine C receptor 7 expression:the role of adenosine receptor A2显示文摘Hypoxia is a major characteristic of the tumor microenvironment,and its effects on immune cells are proposed to be important factors for the process of tumor immune escape.It has been reported that hypoxia affects the function of dendritic cells and the antitumor function of T cells.Here we discuss the effects of hypoxia on T-cell survival.Our results showed that hypoxia induced apoptosis of T cells.Adenosine and adenosine receptors(AR)are important to the hypoxia-related signaling pathway.Using AR agonists and antagonists,we demonstrated that hypoxia-induced apoptosis of T cells was mediated by A^(2a)and A^(2b)receptors.Furthermore,we are the first,to our knowledge,to report that hypoxia significantly inhibited the expression of chemokine C receptor 7(CCR7)of T cells via the A^(2)R signal pathway,perhaps representing a mechanism of hypoxia-induced apoptosis of T cells.Collectively,our research demonstrated that hypoxia induces T-cell apoptosis by the A^(2)R signaling pathway partly by suppressing CCR7.Blocking the A^(2)R signaling pathway and/or activation of CCR7 can increase the anti-apoptosis function of T cells and may become a new strategy to improve antitumor potential. | Jintang Sun Yan Zhang Meixiang Yang Yun Zhang Qi Xie Zewu Li Zhaogang Dong Yongmei Yang Biping Deng Alei Feng Weixu Hu Haiting Mao Xun Qu | 2010 | Cellular & Molecular Immunology2010，7，1： | 3 |
| 2 | Osteopontin splice variants expressed by breast tumors regulate monocyte activation via MCP-1 and TGF-β1显示文摘Osteopontin (OPN ) ,多功能的 glycoprotein,有在 vitro 在肿瘤有不同角色的三个抄本。OPN 抄本是否在 vivo 在肿瘤进程有不同函数,是不清楚的。有免疫力的导出房间的 OPN 能支持肿瘤形成,这被报导了。我们建议导出肿瘤的 OPN 可以便于的一个假设由影响有免疫力的房间区别和功能的肿瘤免疫者逃跑。在这研究,我们构造了 OPN 抄本和 transfected 的 lentiviral 表示向量他们进 MCF-7 房间线。有 OPN 抄本的 MCF-7 房间 transfected 被注入裸体老鼠的腋窝,并且肿瘤生长被监视。结果证明所有 OPN 抄本支持了本地肿瘤形成,而是那在抄本之中没有重要差别。我们也调查了 coculturing 单核白血球肿瘤房间与肿瘤上层清液在单核白血球区别上表示的 OPN 的效果。我们与 OPN 相比发现 OPN-c upregulated CD163 层次 --and OPN-b;然而,任何一个都没抄本影响 HLA 医生和 CD206 层次。所有 OPN 抄本显著地禁止了 TNF-α并且由单核白血球提高了 IL-10 生产。而且,我们发现了 OPN 抄本的 overexpression 显著地 upregulated TGF-β 1 并且由肿瘤房间的 MCP-1 生产。用抵销抗体和 recombinant cytokines,我们发现由肿瘤房间的 OPN overexpressed 调整 TNF-α 的生产;并且由单核白血球的 IL-10 部分经由 MCP-1 和 TGF-β 1 分别地。一起,我们的结果证明 OPN 抄本没在 vivo 在乳癌形成有不同角色。我们也证明 OPN 经由 TGF-β 调整单核白血球的其他的激活; 1 并且 MCP-1,它可以为肿瘤代表另外的机制免疫者逃跑。 | Jintang Sun Alei Feng Songyu Chen Yun Zhang Qi Xie Meixiang Yang Qianqian Shao Jia Liu Qifeng Yang Beihua Kong Xun Qu | 2013 | Cellular & Molecular Immunology2013，10，2： | 2 |
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