Hum. Reprod. Advance Access published online on June 9, 2005
Human Reproduction, doi:10.1093/humrep/dei105
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1 State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, China
* To whom correspondence should be addressed. BACKGROUND: Recent studies suggest a role for interferon-
Received February 20, 2005
Revised March 18, 2005
Accepted April 29, 2005
Article
Effect on expression of RT1-A and RT1-DM molecules of treatment with interferon-
at the maternal--fetal interface of pregnant rats
Jing-Pian Peng, E-mail: pengjp{at}ioz.ac.cn
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Abstract
(IFN-
) in the pregnancy process. METHODS: The expression of non-classical class II major histocompatibility complex (RT1-DM) antigens and classical class I major histocompatibility complex (RT1-A) antigens induced by IFN-
was examined by reverse transcription-PCR, western blotting and immunohistochemistry. RESULTS: IFN-
treatment increased expression of RT1-DM and RT1-A during early pregnancy and decreased them during mid pregnancy at the maternal-fetal interface. In late pregnancy, expression of RT1-A decreased in placenta and increased in uterus, and RT1-DM increased in both placenta and uterus with IFN-
treatment compared with untreated controls. Immunohistochemical studies suggested that in early pregnancy, RT1-DM protein mainly localized to uterine luminal epithelium and glandular epithelium, and RT1-A mainly localized to decidual blood vessels and decidua basalis. During mid and late pregnancy, RT1-A mainly localized in decidual blood vessels and spongiotrophoblast cells of the junction zone. RT1-DM mainly localized in blood vessels and the labyrinthine zone during mid and late gestation. CONCLUSIONS: RT1-A and RT1-DM can both be expressed at the maternal-fetal interface during normal pregnancy. Their localizaion changed according to the period of pregnancy. IFN-
can modulate the expression of these two molecules during the whole pregnancy.
; placenta; RT1-A; RT1-DM; uterus.
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