Abstract

Major histocompatibility class I proteins display viral and self antigens to potentially responsive cells and are important for the maturation of T cells; β 2 -microglobulin (β 2 M) is required for their normal expression. Mouse chimeras derived from embryonic stem cells with a disrupted β 2 M gene transmitted the inactivated gene to their progeny. Animals homozygous for the mutated β 2 M 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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