Regulation of Maternal Anti-Paternal Immune Responses in Vitro by Uterine Macrophages

Abstract

The failure of elements of the maternal immune system to effect rejection of the semiallogeneic fetus remains a major biologic enigma. Currently, the immunologically privileged status of the mammalian embryo is believed to result from 1) failure of expression of histocompatibility antigens by fetal trophoblasts, thus providing an immunologically inert barrier between the mother and the fetus (Simmons and Russell, 1962; Jenkinson and Owen, 1980) and 2) localized immunosuppression in lymph nodes, blood and uterine tissue surrounding the fetus that prevents generation of a cellular immune response (Clark et al., 1984a, 1984b; Hunt et al., 1984b). Two major findings support those hypotheses: 1) trophoblast is poorly or nonstimulatory to lymphocytes (Jenkinson and Billington, 1974; Hunt et al., 1984a) and 2) a cellular immune response to fetal histocompatibility antigens is not generated during pregnancy (Wegmann et al., 1979) although the mother remains generally immunocompetent and antibodies are produced to fetal histocompatibility antigens.