Selective loss of H-2Ds antigen on a murine B lymphoma due to a post-transcriptional block in expression.
Selective loss of H-2Ds antigen on a murine B lymphoma due to a post-transcriptional block in expression.
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由于转录后表达阻断，小鼠 B 淋巴瘤上的 H-2Ds 抗原选择性丢失。
DOI：
10.1016/0161-5890(95)00092-5
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发表时间：
1995
影响因子：
3.6
通讯作者：
King,SR
中科院分区：
文献类型：
--
作者：
Luo,H;Sopchak,L;Lerman,SP;King,SR
主要组织相容性（MHC）I类抗原在大多数细胞中协调表达。然而，一些肿瘤或病毒感染的细胞缺乏一种MHC I类抗原的表达，而其他MHC I类抗原的表达不受影响。我们以前描述了选择性表达的MHC I类抗原的B细胞淋巴瘤从SJL J小鼠称为RCSS。该肿瘤表达H-2Ks，但失去了H-2Ds的细胞表面表达。为了了解H-2D在细胞表面选择性丢失的机制，我们分析了RCS 5肿瘤中的H-2DsmRNA和蛋白。在此我们报道了H-2DsmRNA在RCS 5中表达，但在细胞裂解物中未检测到H-2Ds蛋白。为了确定来自RCSS的H-2DsmRNA是否能够指导H-2Dsprotein的合成，我们使用与RCSS相关的细胞系（cRCS-X）进行cDNA克隆、体外翻译和基因转移实验。我们的结果表明，在cRCS-X中，H-2DsmRNA的表达抑制发生在非缺陷H-2DsmRNA转录后。此外，使用逆转录病毒载体表达重组H-2DscDNA，在cRCS-X中恢复H-2Dsantigen表达。这些结果表明，抑制H-2DsmRNA表达可以克服竞争的抑制剂，反式或通过删除内源性H-2DsmRNA的顺式作用的调控序列。
The major histocompatibility (MHC) class I antigens are coordinately expressed in most cells. However, some tumors or virus-infected cells lack expression of one MHC class I antigen, while expression of the other MHC class I antigens is unaffected. We previously described the selective expression of MHC class I antigens on a B-cell lymphoma from SJL J mice called RCSS. This tumor expresses H-2Ks, but has lost cell surface expression of H-2Ds. To understand the mechanism responsible for the selective loss of H-2Dson the cell surface, we analysed H-2DsmRNA and protein in the RCS5 tumor. Here we report that H-2DsmRNA was expressed in RCS5, but H-2Dsprotein was not detected in cell lysates. To determine whether the H-2DsmRNA from RCSS was able to direct the synthesis of H-2Dsprotein, we performed cDNA cloning, in vitro translation and gene transfer experiments using a cell line related to RCSS (cRCS-X). Our results indicated that the inhibition of H-2Dsexpression in cRCS-X occurred after transcription of a non-defective H-2DsmRNA. Furthermore, H-2Dsantigen expression was restored in cRCS-X using a retroviral vector to express the recombinant H-2DscDNA. These results indicate that the inhibition of H-2Dsexpression could be overcome either by out competing an inhibitor that functions in trans or by removing cis-acting regulatory sequences from the endogenous H-2DsmRNA.