دورية أكاديمية

NF-κB regulation in maternal immunity during normal and IUGR pregnancies.

التفاصيل البيبلوغرافية
العنوان: NF-κB regulation in maternal immunity during normal and IUGR pregnancies.
المؤلفون: Ariyakumar G; Division of Perinatal Medicine, Faculty of Medicine and Health, The University of Sydney, and Northern Sydney Local Health District Research (Kolling Institute), St Leonards, NSW, 2065, Australia., Morris JM; Division of Perinatal Medicine, Faculty of Medicine and Health, The University of Sydney, and Northern Sydney Local Health District Research (Kolling Institute), St Leonards, NSW, 2065, Australia.; Department of Obstetrics and Gynaecology, Royal North Shore Hospital, St Leonards, NSW, 2065, Australia., McKelvey KJ; Bill Walsh Translational Cancer Research Laboratory, Faculty of Medicine and Health, The University of Sydney, and Northern Sydney Local Health District Research (Kolling Institute), St Leonards, NSW, 2065, Australia., Ashton AW; Division of Perinatal Medicine, Faculty of Medicine and Health, The University of Sydney, and Northern Sydney Local Health District Research (Kolling Institute), St Leonards, NSW, 2065, Australia., McCracken SA; Division of Perinatal Medicine, Faculty of Medicine and Health, The University of Sydney, and Northern Sydney Local Health District Research (Kolling Institute), St Leonards, NSW, 2065, Australia. sharon.mccracken@sydney.edu.au.
المصدر: Scientific reports [Sci Rep] 2021 Oct 25; Vol. 11 (1), pp. 20971. Date of Electronic Publication: 2021 Oct 25.
نوع المنشور: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 101563288 Publication Model: Electronic Cited Medium: Internet ISSN: 2045-2322 (Electronic) Linking ISSN: 20452322 NLM ISO Abbreviation: Sci Rep Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : Nature Publishing Group, copyright 2011-
مواضيع طبية MeSH: Fas Ligand Protein/*metabolism , Fetal Growth Retardation/*immunology , Placenta/*metabolism , Th1 Cells/*immunology , Th17 Cells/*immunology , Transcription Factor RelA/*metabolism, Adult ; Cells, Cultured ; Exosomes/metabolism ; Female ; Flow Cytometry ; Humans ; Maternal Age ; Pregnancy ; Pregnancy Trimester, Third/immunology ; Young Adult
مستخلص: Intrauterine Growth Restriction (IUGR) is a leading cause of perinatal death with no effective cure, affecting 5-10% pregnancies globally. Suppressed pro-inflammatory Th1/Th17 immunity is necessary for pregnancy success. However, in IUGR, the inflammatory response is enhanced and there is a limited understanding of the mechanisms that lead to this abnormality. Regulation of maternal T-cells during pregnancy is driven by Nuclear Factor Kappa B p65 (NF-κB p65), and we have previously shown that p65 degradation in maternal T-cells is induced by Fas activation. Placental exosomes expressing Fas ligand (FasL) have an immunomodulatory function during pregnancy. The aim of this study is to investigate the mechanism and source of NF-κB regulation required for successful pregnancy, and whether this is abrogated in IUGR. Using flow cytometry, we demonstrate that p65 + Th1/Th17 cells are reduced during normal pregnancy, but not during IUGR, and this phenotype is enforced when non-pregnant T-cells are cultured with normal maternal plasma. We also show that isolated exosomes from IUGR plasma have decreased FasL expression and are reduced in number compared to exosomes from normal pregnancies. In this study, we highlight a potential role for FasL + exosomes to regulate NF-κB p65 in T-cells during pregnancy, and provide the first evidence that decreased exosome production may contribute to the dysregulation of p65 and inflammation underlying IUGR pathogenesis.
(© 2021. The Author(s).)
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المشرفين على المادة: 0 (FASLG protein, human)
0 (Fas Ligand Protein)
0 (RELA protein, human)
0 (Transcription Factor RelA)
تواريخ الأحداث: Date Created: 20211026 Date Completed: 20220126 Latest Revision: 20230207
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC8545974
DOI: 10.1038/s41598-021-00430-3
PMID: 34697371
قاعدة البيانات: MEDLINE
الوصف
تدمد:2045-2322
DOI:10.1038/s41598-021-00430-3