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γ氨基丁酸对人IL-2和IFN-γ诱导的杀伤细胞的作用研究 被引量:1

Effect of γ-butyric acid on human cytokine IL-2 and IFN-γ-induced killer cells
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摘要 为研究γ氨基丁酸(GABA)及A受体激动剂(THIP)对人细胞因子诱导的杀伤细胞(cytokine-induced killer cell,CIK)的增殖、T细胞亚群和杀瘤活性的影响和作用机制;在体外用不同浓度的GABA和THIP与人CIK细胞作用后,用MTT比色法和流式细胞仪(FCM)以及乳酸脱氢酶(LDH)法分别检测人CIK细胞的增殖能力、T细胞亚群和杀伤活性的变化。结果显示,GABA能显著的抑制CIK细胞的生长(P<0.01),并具有浓度依赖性,THIP对GABA的抑制细胞增殖有明显促进作用;GABA显著降低CIK细胞表面分子CD28分子的表达,降低CD8+T细胞的百分比,抑制CIK细胞对人结肠癌细胞株SW480的杀伤活性,THIP能够增强GABA的作用。上述结果提示,GABA能显著抑制CIK细胞的增殖,降低其细胞表面CD28分子的表达,降低CD8+T细胞的百分比,抑制CIK细胞的杀伤活性,这些作用主要是通过T淋巴细胞上的GABAA受体介导。 To investigate the effect of γ-butyric acid (GABA) and its receptors on proliferation of the human cytokine-induced killer cells (CIK), T cell subsets and anti-tumor activity, CIK cells were cultivated by routine method and then treated with different concentrations of GABA and its receptor agonist THIP. The proliferation of human CIK. T cell subsets and the cytotoxic activity were determined by MTT colorimetry, flow cytometry and lactate dehydrogenase (I.DH) assay respectively. It was a dose-dependent manner (P〈0.01) and the expression of the CD28 molecule on the surface of CIK cells was down-regulated after treatment of these cells with GABA. In addition, GABA could also reduce the percentage of CD8 ^+ T cells and inhibit the cytotoxic activity of CIK cells on cell line SW480 cells from human colon carcinoma. These actions of GABA could be enhanced by receptor agonist THIP. From the above observations, it suggests that these actions may be mediated through the GABA receptor on the surface of T lymphocytes.
出处 《现代免疫学》 CAS CSCD 北大核心 2007年第5期403-406,共4页 Current Immunology
基金 南京军区医学科学技术研究<十一五>计划课题资助项目(06MA45)
关键词 Γ氨基丁酸 CIK细胞 T细胞亚群 杀伤活性 γ-aminobutyric acid cytokine-induced killer cell T lymphocyte cell subsets cytotoxicity
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  • 1张有顺,戴宗晴.肝癌生物治疗研究进展[J].中国现代普通外科进展,2001,4(4):193-196. 被引量:3
  • 2陈复兴 刘军权 等.人PBMC经数种活化剂活化后的表型变化[J].中国肿瘤生物治疗杂志,1999,6:186-187.
  • 3陶义训 章谷生.临床免疫学检验[M].上海:上海科学技术出版社,1983..
  • 4陈复兴 刘军权 等.抗人CD3单克隆抗体体外诱导T细胞和肿瘤浸润性淋巴细胞增殖的研究[J].南京部队医药,1994,5:15-17.
  • 5Schmidt-Wolf IG, Negrin RS, Kiem HP, et al. Use of a SCID mouse/human lymphoma model to evaluate cytokine-induced killer cells with potent antitumor cell activ [ 3 ] Schmidt-Woff GD, Negrin RS,Schmidt-Wolf IG. Activated T cells and cytokine-induced CD3+ CD56+ killer cells[J]. Ann Hematol, 1997,74:51.
  • 6Schmidt-Wolf IC, Lefterova P, Johnston V, et al. Sensitivity of multidrug-resistant tumor cell lines to immunologic effector cells[J]. Cell Immunol, 1996,169:85.
  • 7Hoyle C, Bangs CD, Chang P, et al. Expansion of philadelphia chromosome-negative CD3( + )CD56( + ) cytotoxic cells from chronic myeloid leukemia patients:in vitro and in vivo efficacy in severe combined immunodeficiency disease mice[J]. Blood, 1998,92:3318.
  • 8Schmidt-Wolf IG, Finke S,Trojaneck B, et al. Phase Ⅰ clinical study applying autolognus immunological effector cells transfected with the interleukin-2 gene in patients with metastatic renal cancer , colorectal cancer and lymphoma[J]. Br J Cancer, 1999,81 : 1009.
  • 9Schmidt-Wolf IG, Lefterova P, Mehta BA, et al. Phenotypic characterization and identification of effector cells involved in tumor cell recognition of cytokine-induced killer cells [ J ]. Exp Hematol,1993, 21: 1673.
  • 10Lu PH, Negrin RS. A novel population of expanded human CD3+ CD56+ cells derived from T cells with potent in vivo antitumor activity in mice with severe combined immunodeficiency [J]. J Immunol,1994, 153: 1687.

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