BACKGROUND: Recent studies suggest a role for interferon-gamma (IFN-gamma) 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-gamma was examined by reverse transcription-PCR, western blotting and immunohistochemistry. RESULTS: IFN-gamma 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-gamma 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-gamma can modulate the expression of these two molecules during the whole pregnancy.
BACKGROUND: Recent studies suggest a role for interferon-gamma (IFN-gamma) 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-gamma was examined by reverse transcription-PCR, western blotting and immunohistochemistry. RESULTS:IFN-gamma 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-gamma 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-gamma can modulate the expression of these two molecules during the whole pregnancy.