Department of Pediatrics and Adolescent Medicine, Division of Neonatology, Pediatric Intensive Care and Neuropediatrics, Medical University of Vienna, Vienna, Austria.
J Leukoc Biol. 2013 May;93(5):781-8. doi: 10.1189/jlb.1011525. Epub 2013 Feb 11.
Bacterial and viral infections cause high rates of morbidity and mortality in premature newborns. In the setting of viral infection, pDCs play a key role as strong producers of IFN-α upon TLR9 activation. We analyzed pDC frequency, phenotype, morphology, and function in CB of preterm and term newborns in comparison with adults. Whereas all age groups show similar pDC numbers, BDCA-2, CD123, and TLR9 levels, the expression of BDCA-4 and capacity to produce IFN-α upon TLR9 challenge were decreased significantly in preterm neonates. Furthermore, we show by means of electron microscopy that pDCs from preterm newborns exhibit a distinct, "immature" morphology. Taken together, these findings suggest decreased functionality of pDCs in the premature newborn. The reduced capacity to produce IFN-α is likely to render such infants more susceptible to viral infections.
细菌和病毒感染会导致早产儿高发病率和死亡率。在病毒感染的情况下，pDC 在 TLR9 激活时作为 IFN-α 的强产生者发挥关键作用。我们分析了 CB 中早产儿和足月儿与成人的 pDC 频率、表型、形态和功能。虽然所有年龄组的 pDC 数量、BDCA-2、CD123 和 TLR9 水平相似，但早产儿的 BDCA-4 表达和 TLR9 刺激后产生 IFN-α 的能力显著降低。此外，我们通过电子显微镜显示，早产儿的 pDC 表现出独特的“不成熟”形态。总之，这些发现表明早产儿的 pDC 功能降低。产生 IFN-α 的能力降低可能使这些婴儿更容易受到病毒感染。
