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作 者:刘世育[1] 王营[2] 费素娟[2] 陈复兴[3] 刘军权[3]
机构地区:[1]徐州市第一人民医院消化内科,江苏徐州221002 [2]徐州医学院附属医院消化内科,江苏徐州221002 [3]中国人民解放军第97医院中心实验室,江苏徐州221004
出 处:《山东大学学报(医学版)》2011年第4期25-28,共4页Journal of Shandong University:Health Sciences
摘 要:目的研究γ-氨基丁酸(γ-aminobutyric acid,GABA)及其A受体拮抗剂印防己毒素(picrotoxin,PTX)对人外周血γδT细胞的增殖、细胞表面受体的表达、杀伤活性的影响及其可能的作用机制。方法在体外用不同浓度的GABA和PTX与人γδT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γδT细胞的增殖能力、T细胞表面受体的表达和杀伤活性的变化。结果 GABA能显著地抑制γδT细胞的生长(P<0.01),并具有浓度依赖性,PTX对GABA的抑制细胞增殖有拮抗作用;GABA显著降低γδT细胞表面受体NKG2D的表达,增加γδ-TCR的表达,PTX有轻微的协同作用;GABA抑制了γδT细胞对人胰腺癌细胞株SW1990的杀伤活性,PTX能够拮抗GABA的此项作用。结论这些结果提示GABA可能通过多种途径对γδT细胞发挥作用,其杀伤活性主要由其表面受体NKG2D介导的,并且需要γδT细胞同时表达γδ-TCR和NKG2D两种受体。Objective To research effects of GABA and GABAA receptor antagonist(picrotoxin,PTX) on proliferation,surface receptor expression and cytotoxicity of human peripheral blood γδT cells,and possible mechanism of action.Methods After γδT cells were treated with different concentrations of GABA and PTX,the proliferation,surface receptor expression and cytotoxicity of γδT cells were detected by MTT,flow cytometry and the lactate dehydrogenase method,respectively.Results GABA could decrease proliferation of γδT cells(P0.01) in a dose-dependent manner.Expression of NKG2D on γδT cells was down-regulated by GABA,while TCR-γδ was up-regulated.GABA could inhibit γδT cells from killing the human pancreatic cancer cell line SW1990.PTX had an antagonistic role in the actions of GABA on the proliferation and cytotoxicity of γδT cells,but for surface receptor expression,PTX had a slightly synergistic effect.Conclusion GABA may affect γδT cells via multiple pathways,besides its a receptor.The cytotoxicity of γδT cells is mainly mediated by NKG2D,which may need expressions of both γδTCR and NKG2D.
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