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Eμ-myc转基因不会抑制淋巴瘤前期和淋巴瘤B细胞上的MHC I类分子表达。

MHC class I expression on prelymphomatous and lymphomatous B-cells is not inhibited by an E mu-myc transgene.

作者信息

Algarra I, Silva S, Ljunggren H G

机构信息

Department of Tumor Biology, Karolinska Institutet, Stockholm, Sweden.

出版信息

Eur J Cancer. 1993;29A(2):238-41. doi: 10.1016/0959-8049(93)90182-f.

Abstract

Increased expression of oncogenes from the myc family has been associated with down-regulation of major histocompatibility complex (MHC) class I molecules. In certain models this has been suggested to contribute to tumour progression. Transgenic mice bearing the cellular myc oncogene coupled to the lymphoid-specific immunoglobulin heavy chain enhancer (E mu) develop clonal B lymphoid malignancies early in life. We have asked if expression of such a constitutively activated E mu-myc transgene in BALB/c mice affects MHC class I expression. H-2Kd and Dd expression on prelymphomatous and lymphomatous B-cells as well as newly established pre-B or B lymphoma cell lines derived from E mu-myc transgenic BALB/c mice were analysed. The results reveal no down-regulated or otherwise altered expression of H-2Kd or Dd on any of the cell populations examined. The results are discussed in relation to the myc associated down-regulation of MHC class I molecules observed in other experimental models.

摘要

myc家族癌基因表达的增加与主要组织相容性复合体(MHC)I类分子的下调有关。在某些模型中,这被认为促进了肿瘤进展。携带与淋巴特异性免疫球蛋白重链增强子(Eμ)偶联的细胞myc癌基因的转基因小鼠在生命早期就会发生克隆性B淋巴细胞恶性肿瘤。我们研究了在BALB/c小鼠中这种组成型激活的Eμ-myc转基因的表达是否会影响MHC I类表达。分析了来自Eμ-myc转基因BALB/c小鼠的淋巴瘤前期和淋巴瘤性B细胞以及新建立的前B或B淋巴瘤细胞系上H-2Kd和Dd的表达。结果显示,在所检测的任何细胞群体上,H-2Kd或Dd的表达均未下调或发生其他改变。结合在其他实验模型中观察到的myc相关的MHC I类分子下调对结果进行了讨论。

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