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Fetal and Maternal Transforming Growth Factor-ß1 May Combine to Maintain Pregnancy in Mice¹

The Neuromuscular Research Group, The University of Otago, Dunedin, New Zealand

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-ß1 (TGFß1) and other cytokines are able to breed, bringing this hypothesis into question. The phenotype of TGFß1 null-mutant mice varies with genetic background. We report here that, in outbred mice, the loss of TGFß1- 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 TGFß1^+/– mice that supported TGFß1-deficient fetuses had high levels of TGFß1 in their plasma. Analysis of the amniotic fluids in this line indicated that biologically relevant levels of maternal TGFß1 were present in the TGFß1^–/– fetuses. These data are consistent with maternal and fetal TGFß1 interacting to maintain pregnancy, within immune-competent mothers.

¹ This study was funded by the Health Research Council of New Zealand and the Marsden Fund.

² Correspondence: Ian S. McLennan, Department of Anatomy and Structural Biology, The University of Otago, P.O. Box 913, Dunedin, New Zealand. FAX: 64 3 479 7254; ian.mclennan{at}stonebow.otago.ac.nz

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