German G Gomez, Michelle J Hickey, Richard Tritz, Carol A Kruse
{"title":"用异体活性细胞毒性 T 淋巴细胞筛选出的免疫抗性人类胶质瘤细胞克隆:多种促凋亡因子的下调。","authors":"German G Gomez, Michelle J Hickey, Richard Tritz, Carol A Kruse","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>We previously reported the cellular, functional and cytogenetic characterization of immunoresistant (IR) 13-06-IR29 and 13-06-IR30 human glioma cell clones isolated after immunoselection with alloreactive cytotoxic T lymphocytes (aCTL). Relative to the 13-06-MG parental cells, both clones resisted aCTL lysis at multiple effector to target ratios; the resistant phenotype was maintained for 13-41 cell doublings after cloning and when selective pressure was removed; cross-resistance to other inducers of apoptosis/cell death was also observed (Gomez et al, 2006; Gomez and Kruse, 2007). In this study we further characterize the IR clones for factors that may contribute to the resistance. Data obtained by in-vitro quantitative morphologic and 7-amino actinomycin D flow cytometric assays revealed reduced apoptotic cell death when IR clones were coincubated with aCTL, relative to the parental cells. Since changes in apoptosis were observed, we examined the expression patterns of apoptosis-related genes in several extracts of parental cells and IR clones using pathway-specific cDNA microarray analysis. In general, the apoptotic factors were downregulated in the IR clones. From three separate extracts analyzed separately on microarrays, three factors, ATM, caspases 3 and 8, were statistically downregulated in both IR clones. Immunoblotting of the proteins confirmed the findings. Therefore, a possible mechanism for immunoresistance in gliomas may be achieved by the downregulation of one or more genes in the apoptotic pathway.</p>","PeriodicalId":12503,"journal":{"name":"Gene Therapy and Molecular Biology","volume":"12 1","pages":"101-110"},"PeriodicalIF":0.0000,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597650/pdf/nihms-66860.pdf","citationCount":"0","resultStr":"{\"title\":\"Immunoresistant human glioma cell clones selected with alloreactive cytotoxic T lymphocytes: downregulation of multiple proapoptotic factors.\",\"authors\":\"German G Gomez, Michelle J Hickey, Richard Tritz, Carol A Kruse\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>We previously reported the cellular, functional and cytogenetic characterization of immunoresistant (IR) 13-06-IR29 and 13-06-IR30 human glioma cell clones isolated after immunoselection with alloreactive cytotoxic T lymphocytes (aCTL). Relative to the 13-06-MG parental cells, both clones resisted aCTL lysis at multiple effector to target ratios; the resistant phenotype was maintained for 13-41 cell doublings after cloning and when selective pressure was removed; cross-resistance to other inducers of apoptosis/cell death was also observed (Gomez et al, 2006; Gomez and Kruse, 2007). In this study we further characterize the IR clones for factors that may contribute to the resistance. Data obtained by in-vitro quantitative morphologic and 7-amino actinomycin D flow cytometric assays revealed reduced apoptotic cell death when IR clones were coincubated with aCTL, relative to the parental cells. Since changes in apoptosis were observed, we examined the expression patterns of apoptosis-related genes in several extracts of parental cells and IR clones using pathway-specific cDNA microarray analysis. In general, the apoptotic factors were downregulated in the IR clones. From three separate extracts analyzed separately on microarrays, three factors, ATM, caspases 3 and 8, were statistically downregulated in both IR clones. Immunoblotting of the proteins confirmed the findings. Therefore, a possible mechanism for immunoresistance in gliomas may be achieved by the downregulation of one or more genes in the apoptotic pathway.</p>\",\"PeriodicalId\":12503,\"journal\":{\"name\":\"Gene Therapy and Molecular Biology\",\"volume\":\"12 1\",\"pages\":\"101-110\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2008-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597650/pdf/nihms-66860.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Gene Therapy and Molecular Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gene Therapy and Molecular Biology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
我们以前曾报道过用异体活性细胞毒性 T 淋巴细胞(aCTL)进行免疫选择后分离出的免疫抗性(IR)13-06-IR29 和 13-06-IR30 人类胶质瘤细胞克隆的细胞、功能和细胞遗传学特征。相对于 13-06-MG 亲本细胞,这两个克隆在多种效应因子与靶细胞比率下都能抵抗 aCTL 的裂解;克隆后 13-41 个细胞倍增时,当选择性压力消除后,抗性表型仍能保持;还观察到对其他凋亡/细胞死亡诱导剂的交叉抗性(Gomez 等人,2006 年;Gomez 和 Kruse,2007 年)。在本研究中,我们进一步分析了红外克隆的特征,以寻找可能导致抗性的因素。体外定量形态学和 7-氨基放线菌素 D 流式细胞测定法获得的数据显示,与亲代细胞相比,IR 克隆与 aCTL 共同作用时,细胞凋亡减少。由于观察到了细胞凋亡的变化,我们使用通路特异性 cDNA 微阵列分析法检测了亲代细胞和 IR 克隆的几种提取物中与细胞凋亡相关的基因的表达模式。一般来说,IR 克隆中的凋亡因子表达下调。在微阵列上分别分析的三个提取物中,ATM、caspases 3和8这三个因子在两个IR克隆中都出现了统计意义上的下调。蛋白质的免疫印迹证实了这些发现。因此,胶质瘤免疫抵抗的可能机制可能是通过下调凋亡途径中的一个或多个基因来实现的。
Immunoresistant human glioma cell clones selected with alloreactive cytotoxic T lymphocytes: downregulation of multiple proapoptotic factors.
We previously reported the cellular, functional and cytogenetic characterization of immunoresistant (IR) 13-06-IR29 and 13-06-IR30 human glioma cell clones isolated after immunoselection with alloreactive cytotoxic T lymphocytes (aCTL). Relative to the 13-06-MG parental cells, both clones resisted aCTL lysis at multiple effector to target ratios; the resistant phenotype was maintained for 13-41 cell doublings after cloning and when selective pressure was removed; cross-resistance to other inducers of apoptosis/cell death was also observed (Gomez et al, 2006; Gomez and Kruse, 2007). In this study we further characterize the IR clones for factors that may contribute to the resistance. Data obtained by in-vitro quantitative morphologic and 7-amino actinomycin D flow cytometric assays revealed reduced apoptotic cell death when IR clones were coincubated with aCTL, relative to the parental cells. Since changes in apoptosis were observed, we examined the expression patterns of apoptosis-related genes in several extracts of parental cells and IR clones using pathway-specific cDNA microarray analysis. In general, the apoptotic factors were downregulated in the IR clones. From three separate extracts analyzed separately on microarrays, three factors, ATM, caspases 3 and 8, were statistically downregulated in both IR clones. Immunoblotting of the proteins confirmed the findings. Therefore, a possible mechanism for immunoresistance in gliomas may be achieved by the downregulation of one or more genes in the apoptotic pathway.