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자료유형
학술저널
저자정보
Jia, Hong-Ying (Clinical Molecular Biology Laboratory, the Second Hospital of Shandong University) Liu, Jun-Li (Clinical Molecular Biology Laboratory, the Second Hospital of Shandong University) Yuan, Ming-Zhen (Department of Urology, the Second Hospital of Shandong University) Zhou, Cheng-Jun (Department of Pathology, the Second Hospital of Shandong University) Sun, Wen-Dong (Department of Urology, the Second Hospital of Shandong University) Zhao, Jing-Jie (Clinical Molecular Biology Laboratory, the Second Hospital of Shandong University) Wang, Jue (Central Research Laboratory, the Second Hospital of Shandong University) Liu, Ling (Clinical Molecular Biology Laboratory, the Second Hospital of Shandong University) Luan, Yun (Central Research Laboratory, the Second Hospital of Shandong University)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제16권 제9호
발행연도
2015.1
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3,901 - 3,905 (5page)

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Objective: Our aim was to investigation the roles of MHC class I chain-related gene A(MICA) and natural killer cell group 2D(NKG2D) in human renal cancer cells. Materials and Methods: The expression of membrane MICA (mMICA) on renal cells and NKG2D on NK cells were detected by flow cytometry (FCM); the content of sMICA were detected by enzyme linked immunosorbent assay (ELISA) and the distribution of mMICA on renal tumor tissues by immunohistochemistry; the interaction between MICA and NKG2D was observed by antibody closed method. Results: Our results showed that the expression of mMICA in renal cancer tissues was significantly higher than in controls, where the soluble MICA was not expressed. Cytotoxic activity of NK cells was significantly reduced after exposure to NKG2D and MICA antibodies (P<0.05), and serum containing sMICA can obviously lower the function of NKG2D (P<0.05). Conclusions: The interaction of mMICA and NKG2D play important roles in mediation of cytotoxicity of NK cells in RCC. On the other hand, sMICA may mediate tumor immune escape through down- regulated NKG2D expression.

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