Faculty Research 1990 - 1999


Expression of allogeneic MHC class I antigens by transgenic mouse trophoblast does not interfere with the normal course of pregnancy.

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Base-Sequence, DNA-Primers: ge, Female, Fetal-Development: ge, im, Fetal-Resorption: ge, im, Gene-Expression, Genes-MHC-Class-I, H-2-Antigens: ge, Isoantigens: ge, Male, Maternal-Fetal-Exchange: ge, im, Mice, Mice-Inbred-C57BL, Mice-Transgenic, Polymerase-Chain-Reaction, Pregnancy, Spleen: im, cy, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-NON-P-H-S, Trophoblast: im

JAX Source

Transgenic Res 1998 Sep;7(5):343-55


Mammalian embryos express paternal histocompatibility antigens which make them potential targets for maternal immune responses. Yet, the histoincompatible fetus survives and develops normally. Down regulation of classical MHC antigen expression by trophoblast cells which are in direct contact with maternal circulation has been repeatedly shown. The trophoblast cells are unable to function properly in antigen presentation and do not induce allogeneic rejection reactions. In the present study we have created transgenic mice that express an allogeneic class I transgene whose transcription is controlled by the transferrin receptor promoter. The expression patterns of the transgene product mice from a single transgenic line were studied in each of the typical placental subpopulations. The allogeneic class I antigen was expressed in the allantoic plate region of the trophoblast, and this expression was not restricted to the endothelial region but extended also to the spongiotrophoblast, as well as the major blood vessels and in the endodermal sinuses. In contrast to the normal class I expression, prominent levels of allogeneic H-2 antigens were detected in the labyrinthine trophoblast. The fetal resorption rate in females mated with these transgenic males was not higher then the normal rate, and the embryos survived and developed normally. These data imply that the unusual expression of allogeneic class I antigens in certain trophoblast subpopulations does not affect fetal development.

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