One of the mysteries of pregnancy is why a mother does not reject her fetuses. Cytokine-modulation of maternal-fetal interactions is likely to be important. However, mice deficient in transforming growth factor-β1 (TGFβ1) and other cytokines are able to breed, bringing this hypothesis into question. The phenotype of TGFβ1 null-mutant mice varies with genetic background. We report here that, in outbred mice, the loss of TGFβ1- deficient embryos is influenced by the parity of their mother. This is consistent with the loss of mutants being due to immune rejection. An inbred line of TGFβ1 /− mice that supported TGFβ1-deficient fetuses had high levels of TGFβ1 in their plasma. Analysis of the amniotic fluids in this line indicated that biologically relevant levels of maternal TGFβ1 were present in the TGFβ1−/− fetuses. These data are consistent with maternal and fetal TGFβ1 interacting to maintain pregnancy, within immune-competent mothers.
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