Normal Development of Mice Deficient in β2M, MHC Class I Proteins, and CD8+ T Cells (Reprinted from Science, vol 248, pg 1227-1230, 1990)

被引:0
|
作者
Koller, Beverly H. [1 ]
Marrack, Philippa [2 ]
Kappler, John W. [2 ]
Smithies, Oliver [1 ]
机构
[1] Univ N Carolina, Dept Pathol, Chapel Hill, NC 27599 USA
[2] Natl Jewish Ctr Immunol & Resp Med, Dept Med, Howard Hughes Med Inst Denver, Denver, CO 80206 USA
来源
JOURNAL OF IMMUNOLOGY | 2010年 / 184卷 / 09期
关键词
MAJOR HISTOCOMPATIBILITY COMPLEX; GERM-LINE TRANSMISSION; EMBRYONIC STEM-CELLS; HOMOLOGOUS RECOMBINATION; TRANSPLANTATION ANTIGENS; HLA-A; RECEPTOR; MOUSE; GENE; BETA-2-MICROGLOBULIN;
D O I
暂无
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Major histocompatibility class I proteins display viral and self antigens to potentially responsive cells and are important for the maturation of T cells; beta(2)-microglobulin (beta M-2) is required for their normal expression. Mouse chimeras derived from embryonic stem cells with a disrupted beta M-2 gene transmitted the inactivated gene to their progeny. Animals homozygous for the mutated beta M-2 gene were obtained at expected frequencies after further breeding. The homozygotes appeared normal, although no class I antigens could be detected on their cells and the animals are grossly deficient in CD4(-)CD8(+) T cells, which normally mediate cytotoxic T cell function.
引用
收藏
页码:4592 / 4595
页数:4
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