Fetal and maternal transforming growth factor-beta 1 may combine to maintain pregnancy in mice

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 beta 1) and other cytokines are able to breed, bringing this hypothesis into q...

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Bibliographic Details
Published in:Biology of reproduction 2004-06, Vol.70 (6), p.1614-1618
Main Authors: McLennan, Ian S, Koishi, Kyoko
Format: Article
Language:English
Subjects:
Amniotic Fluid - immunology
Animals
Female
Fetal Blood - immunology
Fetal Death - genetics
Fetal Death - immunology
Maternal-Fetal Exchange - immunology
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Nude
Parity
Pregnancy
Pregnancy Maintenance - immunology
Transforming Growth Factor beta - blood
Transforming Growth Factor beta - deficiency
Transforming Growth Factor beta - genetics
Transforming Growth Factor beta - metabolism
Transforming Growth Factor beta1
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Summary: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 beta 1) and other cytokines are able to breed, bringing this hypothesis into question. The phenotype of TGF beta 1 null-mutant mice varies with genetic background. We report here that, in outbred mice, the loss of TGF beta 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 beta 1(+/-) mice that supported TGF beta 1-deficient fetuses had high levels of TGF beta 1 in their plasma. Analysis of the amniotic fluids in this line indicated that biologically relevant levels of maternal TGF beta 1 were present in the TGF beta 1(-/-) fetuses. These data are consistent with maternal and fetal TGF beta 1 interacting to maintain pregnancy, within immune-competent mothers.
ISSN:0006-3363
DOI:10.1095/biolreprod.103.026179