| First Author | McLennan IS | Year | 2004 |
| Journal | Biol Reprod | Volume | 70 |
| Issue | 6 | Pages | 1614-8 |
| PubMed ID | 14766723 | Mgi Jnum | J:96993 |
| Mgi Id | MGI:3574127 | Doi | 10.1095/biolreprod.103.026179 |
| Citation | McLennan IS, et al. (2004) Fetal and maternal transforming growth factor-beta 1 may combine to maintain pregnancy in mice. Biol Reprod 70(6):1614-8 |
| abstractText | 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. |
