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 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.
McLennan
Ian S
IS
The Neuromuscular Research Group, The University of Otago, Dunedin, New Zealand. ian.mclennan@stonebow.otago.ac.nz
Koishi
Kyoko
K
D000653:Amniotic Fluid / Q000276:immunology; D000818:Animals; D005260:Female; D005312:Fetal Blood / Q000276:immunology; D005313:Fetal Death / Q000235:genetics / Q000276:immunology; D008431:Maternal-Fetal Exchange / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008819:Mice, Nude; D010298:Parity; D011247:Pregnancy; D011255:Pregnancy Maintenance / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000097:blood / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D053773:Transforming Growth Factor beta1
C508961:Tgfb1 protein, mouse; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1