Abstract:

The aim of this study was to investigate MHC expression and localization in uterus and placenta of pregnancy rat, and to study the possible mechanism of immunomodulation classical class Ⅰmajor histocompatibility complex (RT1-A) antigens and non-classical classⅡ major histocompaibility complex (RT1-DM) antigens influenced by exogenous TGF-β1 (Transforming Growth Factor-β1). All of these parameters were examined by western blot and immunohistochemistry. The results showed that the expression of RT1-A and RT1-DM protein were examined in uterus and placenta during every stage of gestation. The expression of RT1-A protein was increasing gradually at uterus during all stage of gestation (D4-D19). The expression of RT1-DM protein was increasing at uterus from early-stage to mid-stage of gestation and decreasing in late-stage. In placenta, the expression of RT1-A, RT1-DM were decreasing gradually during mid-stage to late-stage of gestation. TGF-β1 treatment increased expression of RT1-A and RT1-DM in pre-implantation stage and decreased them in implantation stage (D6-D9) and late at uterus. During late-stage gestation (D19) TGF-β1 treatment significantly inhibited the expression of RT1-A and RT1-DM protein at uterus (P<0.01). The expression of RT1-A and RT1-DM was up-regulated during mid gestation significantly (P<0.05, P<0.01). Immunohistochemistry showed that TGF-β1 did not affect the localization of the two molecules: in early pregnancy RT1-DM mainly localized on uterine luminal epithelium, glandular epithelium, blood vessels, myometrium. RT1-A mainly localized on decidual blood vessels luminal epithelium, glandular epithelium, dicidualbasalis. During mid and late pregnancy, RT1-A and RT1-DM mainly localized on labyrinthine zones, spongiotrophoblast, glandular epithelium, uterus blood vessels. These results indicated that the expression of MHC antigens and TGF-β1 in maternal-fetal interface which may be helpful for constructing an appropriate micro-immunoenvironment of fetal parturition during normal pregnancy.