McLennan Ian S, Koishi Kyoko
The Neuromuscular Research Group, The University of Otago, Dunedin, New Zealand.
Biol Reprod. 2004 Jun;70(6):1614-8. doi: 10.1095/biolreprod.103.026179. Epub 2004 Feb 6.
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.
怀孕的奥秘之一是母亲为何不会排斥自己的胎儿。细胞因子对母婴相互作用的调节可能至关重要。然而，缺乏转化生长因子-β1（TGF-β1）及其他细胞因子的小鼠仍能够繁殖，这使得该假设受到质疑。TGF-β1基因敲除小鼠的表型因遗传背景而异。我们在此报告，在远交系小鼠中，TGF-β1缺陷胚胎的丢失受其母亲生育次数的影响。这与突变体的丢失是由于免疫排斥相符。一个能够支持TGF-β1缺陷胎儿的TGF-β1（+/-）近交系小鼠品系，其血浆中TGF-β1水平很高。对该品系羊水的分析表明，在TGF-β1（-/-）胎儿中存在具有生物学活性的母体TGF-β1水平。这些数据表明，在具有免疫能力的母亲体内，母体和胎儿的TGF-β1相互作用以维持妊娠。
