EMBRYONIC EXPRESSION OF MHC CLASS-I HEAVY AND LIGHT-CHAINS IN TRANSGENIC MICE

被引:16
作者
ISHII, M
TASHIRO, F
HAGIWARA, S
TOYONAGA, T
HASHIMOTO, C
TAKEI, I
YAMAMURA, K
MIYAZAKI, J
机构
[1] UNIV TOKYO,FAC MED,DEPT DIS RELATED GENE REGULAT RES SANDOZ,BUNKYO KU,TOKYO 113,JAPAN
[2] KEIO UNIV,SCH MED,DEPT INTERNAL MED,TOKYO 160,JAPAN
[3] KUMAMOTO UNIV,SCH MED,INST EMBRYOL MOLEC & GENET,KUMAMOTO 862,JAPAN
关键词
TRANSGENIC MOUSE; TOLERANCE; BETA-ACTIN PROMOTER; MHC CLASS I; BETA(2)-MICROGLOBULIN;
D O I
10.1507/endocrj.41.Supplement_S9
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Class I membrane glycoproteins encoded by major histocompatibility complex (MHC) genes are not expressed during early stages of development. This regulation is thought to play an important role in maternal tolerance of the fetal allograft. To elucidate the significance of developmental regulation of MHC class I genes, we produced transgenic mice expressing transgenes encoding the class I L(d) heavy chain or the light chain, beta(2)-microglobulin, in the developing mouse embryo. These transgenes were driven by the chiken beta-actin promoter, which is very active in the developing mouse embryo. The heavy chain and light chain transgenic mice were mated, and the resultant double transgenic offspring expressed L(d) antigen in all the tissues examined by immunostaining and Northern blot analysis. The L(d) antigen was also detected by immunostaining in the placenta of the double transgenic fetus. The double transgenic fetus was not rejected by the immunocompetent nontransgenic mother. These results suggest that expression of MHC class I antigens in embryos is not sufficient to provoke a maternal immune response.
引用
收藏
页码:S9 / S16
页数:8
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