Immunology

Fetal and Maternal Transforming Growth Factor-1 May Combine to Maintain Pregnancy in Mice

Abstract
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-beta1 (TGF-1) and other cytokines are able to breed, which brings this hypothesis into question. The phenotype of TGF-1 null-mutant mice varies with genetic background. We report here that in out-bred mice the loss of TGF-1-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 TGF-1^+/- mice that supported TGF-1-deficient fetuses had high levels of TGF-1 in their plasma. Analysis of the amniotic fluids in this line indicated that biologically relevant levels of maternal TGF-1 were present in the TGF-1^-/- fetuses. These data are consistent with maternal and fetal TGF-1 interacting to maintain pregnancy, within immune-competent mothers.

Key words: Immunology • Pregnancy • Conceptus • Cytokines • Growth factors

This article has been cited by other articles:

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