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The placenta employs a number of mechanisms that protect the embryo/fetus from infection. Genes involved in immune regulation are among the most differentially expressed^{30, 31} and differentially methylated³² in the placenta across different gestational ages. The human placenta is not only the source of hematopoiesis early in pregnancy, but remains a hematopoietic organ throughout gestation.^{33, 34} The placenta also contains a large number of Hofbauer cells (placental macrophages), which may play roles in placental angiogenesis and prevent pathogens crossing from mother to fetus.³⁵ Exosomes and microvesicles also appear to provide protection against viruses, which may be partially attributable to transmission of members of the chromosome 19 placenta‐specific paternally expressed microRNA cluster (C19MC).³⁶ Understanding how the placenta protects from infection is an important question in the study of preterm birth (PTB). Chorioamnionitis (CA), or intra‐amniotic infection, an inflammation of the chorion and amnion usually caused by bacterial infection, is associated with the majority of extremely (<28 weeks) PTBs and about 16 percent of PTBs at 34 weeks.^{37, 38} Genetic variants that modify the maternal or fetal immune response have been linked to risk for PTB and/or PTL^{39, 40} possibly by disrupting cytokine balance (e.g. IL‐6 : IL‐10 ratio).⁴¹