Unexplained spontaneous abortion in humans is currently thought to be related to genetic or immunologic factors. Animal models of spontaneous abortion have been used to try to gain some insight into the problems in humans. From studies of animal models there is increasing evidence that a variety of mechanisms may initiate pregnancy failure and participation of immunologic effectors may be a secondary event. Recent studies indicate that murine abortion that occurs spontaneously (without deliberate immunization by the investigator) may be initiated by para-immunologic host effector cells such as NK cells, macrophages and their toxins that possess selective toxicity which is not antigen-specific. The potential importance of local non-specific suppressive mechanisms in the uterus is also highlighted by their ability to block non-specific paraimmune effector cell activation, and by their potential relationship to growth factors in decidual supernatants that promote placental cell growth in vitro. Levels of non-specific suppression do not appear low when fetal death can be attributed to a genetic mutation. The concept that different tissue components of (Tsutsumi and Oka, 1987). In T cell deficient mice, failure of xenogeneic trophoblast to recruit suppressor cells could also mean failure to recruit non-T cells that elaborate growth factors. Failure of allogeneic trophoblast adequately to recruit cells that elaborate suppressor/growth factors could lead to defective placental development and hence to embryo death.A model summarizing putative host mechanisms damaging fetal and trophoblast tissue is shown in Fig. 1. The data as currently interpreted strongly suggest that further progress will result from investigation of para-immunologic mechanisms in models of spontaneous abortion where the pathogenesis remains unclear. From studies on experimental animal systems one may eventually understand unexplained recurrent abortion in humans, a condition which at present most likely reflects a variety of different pathogenetic mechanisms.
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