Végh Z, Wang P, Vánky F, Hising C, Sjöwall K, Larsson B, Klein E
Department of Tumour Biology, Karolinska Institute, Stockholm, Sweden.
Cancer Immunol Immunother. 1994 Jan;38(1):71-3. doi: 10.1007/BF01517173.
Twenty-nine samples of ex vivo ovarian and lung carcinomas were investigated for the relationship between the presence of mutated protein 53 (mp53) and cytotoxic susceptibility. Unaltered expression of MHC class I alleles was required for the cytotoxic susceptibility of tumour cells to the autologous ex vivo blood lymphocytes, i.e. all 4 sensitive tumours belonged to the group of 11 tumours without defect in MHC class I expression. In contrast, the susceptibility did not correlate with the presence of mp53, i.e. cases with mp53 were randomly distributed between the sensitive and resistant tumours (2/4 and 10/17 respectively). There was no correlation either between the p53 mutation and down-regulation of MHC class I alleles. The results suggest that in these tumours the mutated p53 is not the source of immunogenic peptides and that the lack of recognition of the tumours with mp53 is not caused by a defect in the expression of MHC class I molecules.
对29个离体卵巢癌和肺癌样本进行了研究,以探讨突变蛋白53(mp53)的存在与细胞毒性敏感性之间的关系。肿瘤细胞对自体离体血淋巴细胞的细胞毒性敏感性要求MHC I类等位基因表达未改变,即所有4个敏感肿瘤均属于11个MHC I类表达无缺陷的肿瘤组。相反,敏感性与mp53的存在无关,即有mp53的病例在敏感和耐药肿瘤之间随机分布(分别为2/4和10/17)。p53突变与MHC I类等位基因下调之间也没有相关性。结果表明,在这些肿瘤中,突变的p53不是免疫原性肽的来源,并且对有mp53的肿瘤缺乏识别不是由MHC I类分子表达缺陷引起的。