Normal Development of Mice Deficient in β <sub>2</sub> M, MCClass I Proteins, and CD8 <sup>+</sup> T Cells

Beverly H. Koller(University of North Carolina at Chapel Hill), Philippa Marrack(Howard Hughes Medical Institute), John W. Kappler(Howard Hughes Medical Institute), Oliver Smithies(University of North Carolina at Chapel Hill)
Science
June 8, 1990
Cited by 880

Abstract

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 2M) is required for their normal expression. Mouse chimeras derived from embryonic stem cells with a disrupted beta 2M gene transmitted the inactivated gene to their progeny. Animals homozygous for the mutated beta 2M 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.


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