Selective loss of mouse embryos due to the expression of transgenic major histocompatibility class I molecules early in embryogenesis

Molecular Reproduction and Development
D Aït-AzzouzeneC Kanellopoulos-Langevin

Abstract

Among the numerous hypotheses proposed to explain the absence of fetal rejection by the mother in mammals, it has been suggested that regulation of expression of the polymorphic major histocompatibility complex (MHC) at the fetal-maternal interface plays a major role. In addition to a lack of MHC gene expression in the placenta throughout gestation, the absence of polymorphic MHC molecules on the early embryo, as well as their low level of expression after midgestation, could contribute to this important biologic phenomenon. In order to test this hypothesis, we have produced transgenic mice able to express polymorphic MHC class I molecules early in embryogenesis. We have placed the MHC class la gene H-2Kb under the control of a housekeeping gene promoter, the hydroxy-methyl-glutaryl coenzyme A reductase (HMG) gene minimal promoter. This construct has been tested for functionality after transfection into mouse fibroblast L cells. The analysis of three founder transgenic mice and their progeny suggested that fetoplacental units that could express the H-2Kb heavy chains are unable to survive in utero beyond midgestation. We have shown further that a much higher resorption rate, on days 11 to 13 of embryonic development, is observe...Continue Reading

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Citations

Sep 21, 2002·Proceedings of the National Academy of Sciences of the United States of America·Mikhail G KoloninWadih Arap
Aug 2, 2000·Proceedings of the National Academy of Sciences of the United States of America·K NagarajuP Plotz
Oct 21, 2005·Journal of Reproductive Immunology·Margaret G Petroff
Jul 3, 2003·Médecine sciences : M/S·Stéphane M Caucheteux, Colette Kanellopoulos-Langevin

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