Defective assembly of class I major histocompatibility complex molecules in an embryonic cell line.

Defective assembly of class I major histocompatibility complex molecules in an embryonic cell line.
复制标题

胚胎细胞系中 I 类主要组织相容性复合体分子的组装有缺陷。

DOI:
10.1002/eji.1830210905
复制
发表时间:
1991
影响因子:
5.4
通讯作者:
Robertson,EJ
Robertson,EJ
中科院分区:
医学3区
文献类型:
--
作者:
Bikoff,EK;Otten,GR;Robertson,EJ

文献摘要

相似文献

发育调节的主要组织相容性复合体(MHC)的产物的表达被认为在母体对胎儿同种异体移植物的耐受中起关键作用。在这里,我们分析了一个细胞系(EE 2 H3),来自早期植入后阶段的小鼠胚胎,这是有缺陷的MHC I类组装。为了跟踪单个明确定义的I类产物的表达,我们在人β-肌动蛋白启动子的控制下引入了H-2Dd基因。我们发现转染的EE 2 H3细胞表达大量的H-2Dd重链和β2-微球蛋白,但仅表达少量的H-2Dd表面蛋白。通过添加适当的抗原肽或通过在低温下培养细胞来拯救表面表达。因此,EE 2 H3表现出的表型与使用抗体和补体选择的I类阴性体细胞变体所描述的表型非常相似。然而,一个显着的差异是,在H-2Dd-转染的EE 2 H3细胞的表面表达显着增强响应干扰素治疗。因此,我们鉴定了一种新型I类组装缺陷细胞系。考虑到EE 2 H3是从小鼠胚胎细胞的原代培养物中建立的,没有免疫选择,因此可能代表通常存在于植入后阶段胚胎中的细胞群,这些发现提高了早期发育期间I类表面抗原表达的可能性,可能部分在MHC I类组装水平上进行后期控制。
Developmentally regulated expression of the products of the major histocompatibility complex (MHC) is thought to play a key role in maternal tolerance of the fetal allograft. Here we analyze a cell line (EE2H3), derived from early post‐implantation‐stage mouse embryos, that is defective for MHC class I assembly. To follow expression of a single well‐defined class I product, we introduced the H‐2Ddgene under control of the human β‐actin promoter. We found that the transfected EE2H3 cells expressed abundant levels of H‐2Ddheavy chains and β2‐microglobulin protein, but only small amounts of H‐2Ddsurface protein. Surface expression was rescued by the addition of an appropriate antigenic peptide, or by culturing the cells at low temperature. The phenotype exhibited by EE2H3 is thus remarkably similar to that described for class I‐negative somatic cell variants selected using antibodies and complement. However, a striking difference was that surface expression in H‐2Dd‐transfected EE2H3 cells was markedly enhanced in response to treatment with interferon. Thus, we have identified a novel class I assembly‐defective cell line. Considering that EE2H3 was established from primary cultures of mouse embryo cells without immunoselection, and is therefore likely to represent a cell population normally present in post‐implantation‐stage embryos, these findings raise the possibility that expression of class I surface antigens during early development may in part be controlled post‐translationally at the level of MHC class I assembly.