دورية أكاديمية
Regulatory T cells are paramount effectors in progesterone regulation of embryo implantation and fetal growth.
| العنوان: | Regulatory T cells are paramount effectors in progesterone regulation of embryo implantation and fetal growth. |
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| المؤلفون: | Green ES; Robinson Research Institute, School of Biomedicine, and., Moldenhauer LM; Robinson Research Institute, School of Biomedicine, and., Groome HM; Robinson Research Institute, School of Biomedicine, and., Sharkey DJ; Robinson Research Institute, School of Biomedicine, and., Chin PY; Robinson Research Institute, School of Biomedicine, and., Care AS; Robinson Research Institute, School of Biomedicine, and., Robker RL; Robinson Research Institute, School of Biomedicine, and., McColl SR; School of Biological Sciences, University of Adelaide, Adelaide, South Australia, Australia., Robertson SA; Robinson Research Institute, School of Biomedicine, and. |
| المصدر: | JCI insight [JCI Insight] 2023 Jun 08; Vol. 8 (11). Date of Electronic Publication: 2023 Jun 08. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Society for Clinical Investigation Country of Publication: United States NLM ID: 101676073 Publication Model: Electronic Cited Medium: Internet ISSN: 2379-3708 (Electronic) Linking ISSN: 23793708 NLM ISO Abbreviation: JCI Insight Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Ann Arbor, Michigan : American Society for Clinical Investigation, [2016]- |
| مواضيع طبية MeSH: | Progesterone*/pharmacology , T-Lymphocytes, Regulatory*, Humans ; Pregnancy ; Female ; Animals ; Mice ; Placenta ; Fetal Growth Retardation ; Embryo Implantation/physiology ; Fetal Development |
| مستخلص: | Progesterone (P4) is essential for embryo implantation, but the extent to which the pro-gestational effects of P4 depend on the maternal immune compartment is unknown. Here, we investigate whether regulatory T cells (Treg cells) act to mediate luteal phase P4 effects on uterine receptivity in mice. P4 antagonist RU486 administered to mice on days 0.5 and 2.5 postcoitum to model luteal phase P4 deficiency caused fewer CD4+Foxp3+ Treg cells and impaired Treg functional competence, along with dysfunctional uterine vascular remodeling and perturbed placental development in midgestation. These effects were linked with fetal loss and fetal growth restriction, accompanied by a Th1/CD8-skewed T cell profile. Adoptive transfer at implantation of Treg cells - but not conventional T cells - alleviated fetal loss and fetal growth restriction by mitigating adverse effects of reduced P4 signaling on uterine blood vessel remodeling and placental structure and by restoring maternal T cell imbalance. These findings demonstrate an essential role for Treg cells in mediating P4 effects at implantation and indicate that Treg cells are a sensitive and critical effector mechanism through which P4 drives uterine receptivity to support robust placental development and fetal growth. |
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| فهرسة مساهمة: | Keywords: Embryonic development; Reproductive Biology; T cells; Tolerance |
| المشرفين على المادة: | 4G7DS2Q64Y (Progesterone) |
| تواريخ الأحداث: | Date Created: 20230516 Date Completed: 20230609 Latest Revision: 20230803 |
| رمز التحديث: | 20230803 |
| مُعرف محوري في PubMed: | PMC10393240 |
| DOI: | 10.1172/jci.insight.162995 |
| PMID: | 37191999 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 2379-3708 |
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| DOI: | 10.1172/jci.insight.162995 |