Browsing by Subject "Fetal Diseases"

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    Flow cytometric methods for prenatal and neonatal diagnosis.
    (J Immunol Methods, 2011-01-05) Curtis, Michèle G; Walker, Brooke; Denny, Thomas N
    Flow cytometry offers a promising alternative to the current methods of amniocentesis or chorionic villus sampling (CVS) for fetal cell sorting for prenatal diagnosis. While flow cytometric methods have been greatly improved to be more sensitive at detecting fetal cells within the maternal circulation, there are still several challenges that need to be overcome before application in prenatal diagnosis. However, flow cytometry is a powerful tool that can be used to enhance molecular testing and other diagnostic testing modalities in prenatal and neonatal diagnosis. It remains the gold standard to identify cellular immunodeficiencies and, for some immunological disorders with established biomarkers, flow cytometric assays can be used to make a definitive diagnosis. In this review, the advantages and disadvantages of using MACS and FACS analysis for fetal cell sorting are discussed. This review also includes an overview of the current flow cytometric assays and biomarkers that may be used for prenatal and neonatal diagnosis of common immunological and hematological abnormalities and the role of flow cytometry in treatment monitoring after bone marrow and stem cell transplantation.
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    Gestational Stage and IFN-λ Signaling Regulate ZIKV Infection In Utero.
    (Cell host & microbe, 2017-09) Jagger, Brett W; Miner, Jonathan J; Cao, Bin; Arora, Nitin; Smith, Amber M; Kovacs, Attila; Mysorekar, Indira U; Coyne, Carolyn B; Diamond, Michael S
    Although Zika virus (ZIKV)-induced congenital disease occurs more frequently during early stages of pregnancy, its basis remains undefined. Using established type I interferon (IFN)-deficient mouse models of ZIKV transmission in utero, we found that the placenta and fetus were more susceptible to ZIKV infection at earlier gestational stages. Whereas ZIKV infection at embryonic day 6 (E6) resulted in placental insufficiency and fetal demise, infections at midstage (E9) resulted in reduced cranial dimensions, and infection later in pregnancy (E12) caused no apparent fetal disease. In addition, we found that fetuses lacking type III IFN-λ signaling had increased ZIKV replication in the placenta and fetus when infected at E12, and reciprocally, treatment of pregnant mice with IFN-λ2 reduced ZIKV infection. IFN-λ treatment analogously diminished ZIKV infection in human midgestation fetal- and maternal-derived tissue explants. Our data establish a model of gestational stage dependence of ZIKV pathogenesis and IFN-λ-mediated immunity at the maternal-fetal interface.