Lack of class I major histocompatibility antigens on trophoblast of periimplantation blastocysts and term placenta in the pig.

In this study, the pattern of expression of class I major histocompatibility (MHC) antigens and mRNA on periimplantation blastocysts and term placental tissue was determined for the pig. Class I MHC antigens could not be detected immunohistochemically either on extra-embryonic membranes or on the embryonic portion of Day 14, 16, 22, and 25 blastocysts. Nor could class I MHC antigens be detected on the outer trophoblast epithelium and inner endodermal surface of the chorioallantoic membrane or on the outer and inner surfaces of the amnion at term.

A progesterone-dependent immunomodulatory protein alters the Th1/Th2 balance.

In the presence of progesterone, lymphocytes from pregnant females produce an immunomodulatory protein known as progesterone induced blocking factor (PIBF). We tested the effect of this protein on cytokine production by mitogen-activated lymphocytes. Spleen cells from Balb/c mice were incubated with Con A in the presence or absence of PIBF.

T helper 1 response against Leishmania major in pregnant C57BL/6 mice increases implantation failure and fetal resorptions. Correlation with increased IFN-gamma and TNF and reduced IL-10 production by placental cells.

Maternal immune responses can influence fetal survival and several cytokines have harmful or protective effects on pregnancy. The Th1 cytokines IFN-gamma and IL-2 can cause fetal loss, whereas the Th2 cytokine IL-10 is protective. However, infections such as leishmaniasis show the opposite pattern: resistance is associated with the preferential mounting of a Th1 response, whereas a Th2 response exacerbates the disease.

Pregnancy impairs resistance of C57BL/6 mice to Leishmania major infection and causes decreased antigen-specific IFN-gamma response and increased production of T helper 2 cytokines.

Resolution of cutaneous leishmaniasis in infected mice is associated with a polarized Th1 immune response by the host, whereas maternal immune responses during pregnancy appear to be biased toward humoral (Th2) and away from cell-mediated (Th1) responses. The objective of this study was to evaluate whether the putative Th2 bias in pregnant C57BL/6 mice would impair their normal ability to mount a curative Th1 response against Leishmania major infection. Pregnant C57BL/6 mice developed larger cutaneous lesions that showed no signs of resolution up to 70 days after infection.