A gene required for class II-restricted antigen presentation maps to the major histocompatibility complex.
A gene required for class II-restricted antigen presentation maps to the major histocompatibility complex.
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DOI：
10.1084/jem.174.6.1607
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发表时间：
1991-12-01
期刊：
影响因子：
--
通讯作者：
Pious D
中科院分区：
文献类型：
--
作者：
Mellins E;Kempin S;Smith L;Monji T;Pious D
我们之前已经描述了一组B淋巴母细胞样细胞系的突变体（16.23个选择的突变体），它们在向ii类限制性T细胞呈递完整蛋白方面存在缺陷，但能有效呈递免疫原性肽。这些突变体的突变在体细胞杂交体中是隐性的，而不是在II类结构基因中。在这里，我们报道了一个独特的突变，5.2.4，其中II类限制性抗原呈递的类似缺陷与主要组织相容性复合体（MHC） II类区域的百万碱基纯合缺失有关。在16.23个选择的突变体中，三个突变体之间以及这些突变体与5.2.4突变体之间的II类缺陷在体细胞杂交种中是不互补的。这表明，所有四种突变体的II类表现缺陷表型都是由单个MHC相关基因的病变引起的，在与第二个无关的MHC缺失突变体T2组成的杂交体中，16.23选择突变体的II类表现缺陷也没有得到补充，这一发现加强了这一结论。突变体5.2.4除了存在II类呈递缺陷外，MHC I类分子的表面表达也存在缺陷，这很可能是因为它缺失了肽供应因子1基因，该基因的功能已知是细胞表面I类分子正常丰度所必需的。然而，在16.23个选择的突变体中，I类分子的表面丰度是正常的，这表明影响I类表面丰度和II类表现的病变是由不同基因的突变引起的。
We have previously described a set of mutants (16.23-selected mutants) of a B lymphoblastoid cell line that are defective in the presentation of intact proteins to class II-restricted T cells, but effectively present immunogenic peptides. The mutations in these mutants are recessive in somatic cell hybrids and are not in Class II structural genes. Here, we report on a unique mutant, 5.2.4, in which a similar defect in class II-restricted antigen presentation has occurred in association with a one-megabase homozygous deletion in the class II region of the major histocompatibility complex (MHC). The defects in class II presentation among three of the 16.23-selected mutants, and between these mutants and 5.2.4, are noncomplementary in somatic cell hybrids. This suggests that the class II presentation-defective phenotype in all four mutants results from lesions in a single MHC- linked gene, a conclusion strengthened by the finding that in a hybrid made with a second, unrelated MHC deletion mutant, T2, the class II presentation defect in a 16.23-selected mutant is also not complemented. Mutant 5.2.4, in addition to its class II presentation defect, is also defective in surface expression of MHC class I molecules, most likely because its deletion encompasses the peptide supply factor 1 gene, whose function is known to be required for normal abundance of cell surface class I molecules. However, the surface abundance of class I molecules is normal in the 16.23-selected mutants, suggesting that the lesions affecting class I surface abundance and class II presentation result from mutations in different genes.
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DOI：
10.1073/pnas.82.23.8183
发表时间：
1985-01-01
影响因子：
11.1
作者：
DEMARS, R;RUDERSDORF, R;ORR, HT
通讯作者：
ORR, HT
影响因子：
64.8
作者：
GLADSTONE, P;PIOUS, D
通讯作者：
PIOUS, D
DOI：
10.1073/pnas.81.13.3934
发表时间：
1984-01-01
期刊：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子：
--
作者：
GORSKI, J;ROLLINI, P;MACH, B
通讯作者：
MACH, B
影响因子：
2.7
作者：
MELLINS, E;WOELFEL, M;PIOUS, D
通讯作者：
PIOUS, D
使用小鼠单克隆抗体对DR3特异的小分子量（β）亚基的HLA-DR同型决定因素的直接证明。
影响因子：
15.3
作者：
Johnson, J P;Meo, T;Riethmuller, G;Schendel, D J;Wank, R
通讯作者：
Wank, R