Synergistic interplay of immune endocrine interaction is prerequisite for an effective maternal fetal tolerance. Pre-term birth (PTB) may be a consequence of altered immune-endocrine crosstalk during third trimester resulting in early breakdown of this tolerance. Myeloid derived suppressor cells (MDSCs), a heterogenous population of immature immune cells are increased in pregnant women and healthy newborns, but their role in PTB still remains obscure. We now report that granulocytic MDSCs (G-MDSCs) is decreased in women delivering prematurely, suggesting their potential role in maintaining maternal fetal tolerance. Interestingly, in contrast statistically significant increase in MDSCs and monocytic MDSCs (M-MDSCs) along with positive correlation with cord serum estradiol (E2), and overexpressed ER-α in placental tissue suggested E2 mediated accumulation of M-MDSCs in PTB babies. MDSCs mediated immune suppression is accompanied with subsequent decline in total T cells and its subtypes: Th and Tc in PTB babies, which signifies their potential contribution towards the impaired immune system of PTB babies.

免疫内分泌相互作用的协同相互作用是有效母胎耐受的先决条件。早产 (PTB) 可能是妊娠晚期免疫内分泌串扰改变的结果，导致这种耐受性的早期破坏。骨髓来源的抑制细胞 (MDSCs) 是一种异质的未成熟免疫细胞群，在孕妇和健康新生儿中有所增加，但它们在 PTB 中的作用仍不清楚。我们现在报道，过早分娩的女性粒细胞 MDSCs (G-MDSCs) 减少，这表明它们在维持母胎耐受中的潜在作用。有趣的是，相比之下，MDSCs 和单核细胞 MDSCs (M-MDSCs) 的显着增加以及与脐带血清雌二醇 (E2) 的正相关，并且胎盘组织中过表达的 ER-α 表明 E2 介导了 PTB 婴儿中 M-MDSC 的积累。MDSCs 介导的免疫抑制伴随着总 T 细胞及其亚型的随后下降：PTB 婴儿中的 Th 和 Tc，这表明它们对 PTB 婴儿免疫系统受损的潜在贡献。