在哺乳动物妊娠期内，母亲和胎儿经常通过胎盘交换关键的化学信号、营养和其他分子。为了实现一个成功的妊娠（其标准是产下健康的后代），母亲必须在免疫学的层次上耐受胎儿组织。没有免疫抑制，胎儿和胎盘将被视为外来组织，被免疫系统攻击，导致妊娠以流产结束。
Derek Wildman及其同事提出，这种类型的耐受是在哺乳动物发展的早期进化出的。这组科学家研究了一种称为galectin-1的抗炎症蛋白的结构，这种蛋白是在子宫等免疫反应受到抑制的“免疫赦免”区域发现的。在研究了来自包括几种灵长类动物在内的数种脊椎动物的该蛋白质后，这组作这发现了这种蛋白结构在有胎盘类哺乳动物的进化过程中是高度保守的。这组科学家提出，galectin-1结构的关键修改——这种修改可以让它执行其免疫功能——是在进化的早期出现的。相关论文发表在美国《国家科学院院刊》（PNAS）上。（生物谷Bioon.com）
生物谷推荐原始出处：
PNAS，doi: 10.1073/pnas.0807606105，Nandor Gabor Than，Derek E. Wildman
Emergence of hormonal and redox regulation of galectin-1 in placental mammals: Implication in maternal–fetal immune tolerance
Nandor Gabor Than, Roberto Romero, Offer Erez, Amy Weckle, Adi L. Tarca, John Hotra, Asad Abbas, Yu Mi Han, Sung-Su Kim, Juan Pedro Kusanovic, Francesca Gotsch, Zhuocheng Hou, Joaquin Santolaya-Forgas, Kurt Benirschke, Zoltan Papp, Lawrence I. Grossman, Morris Goodman, and Derek E. Wildman
Galectin-1 is an anti-inflammatory lectin with pleiotropic regulatory functions at the crossroads of innate and adaptive immunity. It is expressed in immune privileged sites and is implicated in establishing maternal–fetal immune tolerance, which is essential for successful pregnancy in eutherian mammals. Here, we show conserved placental localization of galectin-1 in primates and its predominant expression in maternal decidua. Phylogenetic footprinting and shadowing unveil conserved cis motifs, including an estrogen responsive element in the 5′ promoter of LGALS1, that were gained during the emergence of placental mammals and could account for sex steroid regulation of LGALS1 expression, thus providing additional evidence for the role of galectin-1 in immune–endocrine cross-talk. Maximum parsimony and maximum likelihood analyses of 27 publicly available vertebrate and seven newly sequenced primate LGALS1coding sequences reveal that intense purifying selection has been acting on residues in the carbohydrate recognition domain and dimerization interface that are involved in immune functions. Parsimony- and codon model-based phylogenetic analysis of coding sequences show that amino acid replacements occurred in early mammalian evolution on key residues, including gain of cysteines, which regulate immune functions by redox status-mediated conformational changes that disable sugar binding and dimerization, and that the acquired immunoregulatory functions of galectin-1 then became highly conserved in eutherian lineages, suggesting the emergence of hormonal and redox regulation of galectin-1 in placental mammals may be implicated in maternal–fetal immune tolerance.
