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Tumor–associated antigens identified by mRNA expression profiling as tumor rejection epitopes

机译:通过mRNA表达谱鉴定为肿瘤排斥抗原的肿瘤相关抗原

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Thirteen H-2b-binding peptides derived from six potentially overexpressed proteins in p53-/- thymoma (SM7) cells were studied for immunogenecity and vaccine-induced prevention of tumor growth in mice inoculated with SM7 tumor cells. Six of the peptides generated specific CTL responses after immunization, but only two of these peptides (RAD23–31 and RAD24–31) were capable of generating a weak vaccination-induced protection against adoptive tumor growth. SM7 inoculated mice treated with a blocking antibody against the inhibitory T cell signal transducing molecule CTLA4 appeared to delay tumor take, suggesting that SM7 thymoma cells are recognized by the adaptive immune system of the host. However, prophylactic vaccination with RAD23–31 and RAD24–31 peptides combined with anti-CTLA4 Ab treatment and did not improve tumor resistance. Our data would indicate that vaccination with immunogenic peptides derived from potentially overexpressed tumor proteins, as identified by mRNA expression profiling of p53-/- thymoma cells, at best results in a weak tumor protection thus questioning this way of detection of new tumor rejection epitopes.
机译:研究了从p53-/-胸腺瘤(SM7)细胞中六个潜在过度表达的蛋白质衍生的13种H-2b结合肽在接种SM7肿瘤细胞的小鼠中的免疫原性和疫苗诱导的肿瘤生长预防作用。六种肽在免疫后产生特定的CTL反应,但是这些肽中只有两种(RAD23-31和RAD24-31)能够产生弱的疫苗接种诱导的针对过继性肿瘤生长的保护作用。用针对抑制性T细胞信号转导分子CTLA4的阻断抗体处理的SM7接种小鼠似乎延迟了肿瘤摄取,表明SM7胸腺瘤细胞被宿主的适应性免疫系统识别。但是,RAD23–31和RAD24–31肽的预防性疫苗接种与抗CTLA4 Ab治疗相结合,并不能改善肿瘤抵抗力。我们的数据表明,用p53-/-胸腺瘤细胞的mRNA表达谱鉴定的潜在潜在过表达的肿瘤蛋白衍生的免疫原性肽的疫苗接种最多只能导致较弱的肿瘤保护,因此对这种检测新肿瘤排斥表位的方式提出了质疑。

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