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Article
Nature 344, 742 - 746 (19 April 1990); doi:10.1038/344742a0

bold beta2-Microglobulin deficient mice lack CD4-8+ cytolytic T cells

Maarten Zijlstra, Mark Bix*, Neil E. Simister, Janet M. Loring, David H. Raulet* & Rudolf Jaenisch

Whitehead Institute for Biomedicai Research, Nine Cambridge Center, and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA
* Center for Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA

Mice homozygous for a beta2-microglobulin gene disruption do not express any detectable beta2-ITL protein. They express little if any functional major histocompatibility complex (MHC) class I antigen on the cell surface yet are fertile and apparently healthy. They show a normal distribution of bold gammadelta, CD4+8+ and CD4+8- cells, but have no mature CD4-8+ cells and are defective in CD4-8+ cell-mediated cytotoxicity. Our results strongly support earlier evidence that MHC class I molecules are crucial for positive selection of T cell antigen receptor alphabeta+ CD4-8+ T cells in the thymus and call into question the non-immune functions that have been ascribed to MHC class I molecules.

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