期刊文献+

氧化应激可选择性诱导细胞的NKG2D配体的表达 被引量:2

Expressions of NKG2D ligands can be selectively induced by oxidative stress
下载PDF
导出
摘要 目的探讨氧化应激与细胞NKG2D配体表达的关系,分析氧化应激对NK细胞功能的影响。方法加H2O2诱导培养的肿瘤细胞处于氧化应激状态。用RT-PCR、Real-time PCR和流式细胞仪等方法分析细胞多种NKG2D配体的表达。用CCK-8法检测NK92细胞对肿瘤细胞的杀伤活性。结果氧化应激可诱导肿瘤细胞多种NKG2D配体的表达,不同的肿瘤细胞诱导表达的NKG2D配体不同;NKG2D配体表达上调可有效提高NK细胞的细胞毒活性,此效应可被抗NKG2D抗体所阻断。结论NKG2D配体可能在机体的免疫应答中发挥正向的调节作用。 Objective To study the relationship between the expression of NKG2D ligands and oxidative stress, and to analyze the effect of oxidative stress on the function of NK cells. Methods Tumor ceils were cultured and exposed to hydrogen peroxide to develope an oxidative stress model. Then to detect the expression of NKG2D ligands in cells by Real-time PCR and Flow Cytometry. The cytotoxieity of NK ceils to tumor cells was detected and compared by CCK-8 kit before and after oxidative stress. Results The expression of NKG2D ligands was induced by oxidative stress,however the NKG2D ligands induced was variable. The up-regulation of NKG2D ligands increased the cytotoxieity of NK ceils efficiently, and this effect was blocked by anti-NKG2D antibody. Conclusion The expression of NKG2D ligands can be selectively induced by oxidative stress on tumor cells, and the improvement of the cytotoxicity of NK cells may enhance the immune responses accordingly.
出处 《基础医学与临床》 CSCD 北大核心 2009年第8期789-795,共7页 Basic and Clinical Medicine
基金 国家自然基金项目(30872362 30490244) 国家高技术研究发展计划(863)项目(2006AA02Z432)
关键词 氧化应激 NKG2D配体 NK细胞 细胞毒活性 oxidative stress NKG2D ligands NK cells cytotoxicity
  • 相关文献

参考文献7

  • 1Mistry AR, O'Callaghan CA. Regulation of ligands for the activating receptor NKG2D [J]. Immunology, 2007, 121: 439 - 447.
  • 2Cosman D, Mullberg J, Sutherland C, et al. ULBPs, novel MHC class I-related molecules, bind to CMV glycoprotein UL16 and stimulate NK cytotoxieity through the NKG2D receptor [J]. Immunity, 2001, 14(2) : 123 - 133.
  • 3Kubin M, Cassiano L, Chalupny J, et al. ULBP1, 2, 3: novel MHC class Z-related molecules that bind to human cytomegalovirus glycoprotein UL16, activate NK cells [ J]. Eur J Immunol, 2001, 31 : 1428 - 1437.
  • 4Pende D, Rivera P, Marcenaro S, et al. Major histoeompatibility complex class 1-related chain A and UL16-bindingprotein expression on tumor cell lines of different histotypes: analysis of tumor susceptibility to NKG2D-dependent natural killer cell cytotoxicity [ J]. Cancer Res, 2002, 62 : 6178 - 6186.
  • 5Raulet DH. Interplay of natural killer cells and their receptors with the adaptive immune response [ J ]. Nat Immunol, 2004, 5 : 996 - 1002.
  • 6Gasser S, Orsulie S, Brown EJ, et al. The DNA damage pathway regulates innate immune system ligands of the NKG2D receptor [J]. Nature, 2005, 436: 1186-1190.
  • 7Ermak G, Davies KJ. Calcium and oxidative stress: from cell signalingto cell death [ J ]. Mol Immunol, 2002, 38 : 713 -721.

同被引文献14

  • 1Mistry AR, O'Callaghan CA. Regulation of ligands for the activating receptor NKG2D [ J ]. Immunology, 2007, 121 : 439 - 447.
  • 2Chen Yongyan, Wei Haiming, Sun Rui, et al. Increased susceptibility to liver injury in hepatitis B virus transgenic mice involves NKG2D-ligand interaction and natural killer cells [J]. Hepatotogy, 2007, 46(3) : 706 -715.
  • 3Arapovic J, Rovis TL, Reddy AB, et al. Promiscuity of MCMV immunoevasin of NKG2D: m138/fcr-1 down-modulates RAE-lepsilon in addition to MULT-1 and H60 [ J ]. Molecular immunology, 2009, 47( 1 ) : 114 - 122.
  • 4Feng Rentian, He Wei, Ochi H, et al. Ozone exposure impairs antigen-specific immunity but activates IL-7-induced proliferation of CD4-CD8-thymocytes in BALB/c mice [J]. J Toxicol Environ Health A, 2006, 69(16) : 1511 -1526.
  • 5Nice TJ, Coscoy L, Raulet DH. Posttranslational regulation of the NKG2D ligand Multl in response to cell stress [ J]. J Exp Med, 2009, 206 (2) : 287 - 298.
  • 6Tomoda A,Joudoi T,Rabab el-M,et al.Cytokine produc-tion and modulation:comparison of patients with chronic fa-tigue syndrome and normal controls[J].Psychiatry Res,2005,134:101-104.
  • 7Borchers MT,Harris NL,Wesselkamper SC,et al.NKG2D ligands are expressed on stressed human airway ep-ithelial cells[J].Am J Physiol Lung Cell Mol Physio,2006,291:L222-231.
  • 8Holgate ST,Komaroff AL,Mangan D,et al.Chronic fa-tigue syndrome:understanding a complex illness[J].NatRev Neurosci,2011,12:539-544.
  • 9Rosenblum H,Shoenfeld Y,Amital H,et al.The commonimmunogenic etiology of chronic fatigue syndrome:from in-fections to vaccines via adjuvants to the ASIA syndrome[J].Infect Dis Clin North Am,2011,25:851-863.
  • 10Meeus M,Nijs J,Truijen S,et al.Role of psychologicalaspects in both chronic pain and in daily functioning inchronic fatigue syndrome:a prospective longitudinal study[J].Clin Rheumatol,2012,DOI 10.1007/s10067-012-1946-z.

引证文献2

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部