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目的 研究曲古菌素A(TSA)诱导Raji细胞和HL-60细胞表达共刺激分子CD80和CD86及其与免疫应答的关系.方法 采用MTT法观察不同浓度TSA对Raji细胞和HL-60细胞的抑制作用,流式细胞仪检测150 nmol/L TSA作用Raji细胞和HL-60细胞的细胞活力及表达共刺激分子CD80和CD86,RT-PCR分析150 nmol/LTSA作用Raji细胞和HL-60细胞CD80和CD86 mRNA表达情况.结果 TSA对Raji细胞和HL-60细胞的抑制作用具有时间和剂量依赖性,流式细胞仪检测Raji细胞培养12、24、48 h表达CD80分别为(76.2±4.6)％、(78.7±6.9)％、(79.2±3.4)％,CD86表达极低,150 nmol/L TSA作用Raji细胞12、24、48 h后,可提高Raji细胞表达CD80,分别为[(82.4±7.2)％,t =2.56,P =0.047]、[(84.8土5.6)％,t=2.57,P=0.042]、[(93.9±8.7)％,t=2.67,P=0.038],CD86不上调;RT-PCR检测Raji细胞表达CD80 mRNA对照组条带亮度为0.45±0.32,150 nmol/L TSA作用Raji细胞12、24、48 h后表达CD80 mRNA增强,分别为(0.49±0.22,t=2.45,P =0.047),(0.76 ±0.33,t=3.67,P=0.0071),(0.85±0.34,t=4.25.P=0.0048).CD86 mRNA不升高.流式细胞仪检测HL-60细胞12、24、48 h表达CD86分别为(28.8±5.3)％、(29.6±6.3)％、(29.2±1.4)％,CD80表达极低,150 nmol/LTSA作用HL-60细胞12、24、48 h后,提高HL-60细胞表达CD86,分别为[(38.5±4.3)％,t=2.87,P=0.037]、[(42.9±7.1)％,t=3.01,P=0.032]、[(61.4±9.7)％,t=4.56,P=0.0076],CD80不上调.RT-PCR检测HL-60细胞表达CD86 mRNA对照组为0.52 ±0.16,150 nmol/L TSA作用HL-60细胞12、24、48 h后表达CD86mRNA增强,分别为(0.63±0.45,t=2.67,P=0.042),(0.75 ±0.61,t=3.97,P=0.0078),(0.92±0.36,t=5.01,P=0.0032),CD80 mRNA不升高.结论 TSA可诱导Raji细胞表达共刺激分子CD80及诱导HL-60细胞表达共刺激分子CD86,促进细胞的免疫应答,为抗恶性血液病提供了一个新的免疫治疗方法.“,”Objective To investigate trichostatin A (TSA)-induced costimulatory molecular C D80 and CD86 expressions of Raji and HL-60 cells as well as the relationship with immune response.Methods The proliferative activities of Raji cells and HL-60 cells were assessed by morphology and methyl thiazolyl tetrazolium (MTT) assay.The expressions of CD80 and CD86 were confirmed,and cell viability was examined by flow cytometer after 150 nmol/L TSA treatment.The expression status of CD80 mRNA and CD86 mRNA was analyzed by reverse transcription polymerase chain reaction (RT-PCR).Results A time-and dose-dependent inhibition was detected in Raji cells and HL-60 cells treated with TSA.The expression of CD80 in Raji cells for 12,24,and 48 h was (76.2 ± 4.6) ％,(78.7 ± 6.9) ％,and (79.2 ± 3.4) ％,respectively.After TSA (150 nmol/L) treatment for 12h,24h,and 48 h,the expression of CD80 was [(82.4±7.2)％,t =2.56,P =0.47],[(84.8 ±5.6)％,t =2.57,P =0.42],and [(93.9 ± 8.7) ％,t =2.67,P =0.38] in Raji cells,respectively.The CD80 mRNA expression was 0.45 ± 0.32 in control group.After TSA (150 nmol/L) treatment in Raji cells for 12,24,and 48h,the CD80 mRNA expression was (0.49 ± 0.22,t =2.45,P =0.47),(0.76 ± 0.33,t =3.67,P =0.0071),and (0.85 ± 0.34,t =4.25.P =0.0048),respectively.The expression of CD86 in HL-60 cells for 12h,24h,and 48 h was (28.8 ± 5.3) ％,(29.6 ± 6.3) ％,and (29.2 ± 1.4) ％.After TSA (150 nmol/L) treatment for 12,24,and48 h,the expression of CD86 was [(38.5 ±4.3)％,t =2.87,P =0.37],[(42.9 ± 7.1) ％,t =3.01,P =0.32],and [(61.4 ± 9.7) ％,t =4.56,P =0.0076],respectively.The CD86 mRNA expression was 0.52 ±0.16 in control group.After TSA (150 nmol/L) treatment in HL-60 cells for 12h,24h,and 48 h,the CD86 mRNA expression was (0.63 ± 0.45,t =2.67,P =0.42),(0.75 ± 0.61,t =3.97,P =0.0078),and (0.92 ±0.36,t =5.01,P =0.0032),respectively.Conclusions TSA induces costimulatory molecular CD80 and CD86 expression of Raji and HL-60 cells,improves immune response of cells,and provides a novel immunotherapy of ant-malignancy hematological disease.