Decreased number of myeloid-derived suppressor cells in the placental trophoblast of gestational diabetes mellitus. Possible role of leptin
Gestational diabetes mellitus (GDM) is the most common complication of pregnancy and significantly increases both maternal and fetal morbidity and mortality. Inflammation is a hallmark of GDM, and placental inflammation may play a key role in the pathophysiology of the disease. Myeloid-derived suppr...
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Elsevier
2025-05-01
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| Series: | Immunobiology |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0171298525000312 |
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| author | Malika Tami Lourdes Hontecillas-Prieto Daniel García-Domínguez Rocío Flores-Campos Teresa Vilariño-García Flora Sánchez-Jiménez Pilar Guadix José L. Dueñas Carlos Jiménez-Cortegana Luis de la Cruz-Merino Antonio Pérez-Pérez Víctor Sánchez-Margalet |
| author_facet | Malika Tami Lourdes Hontecillas-Prieto Daniel García-Domínguez Rocío Flores-Campos Teresa Vilariño-García Flora Sánchez-Jiménez Pilar Guadix José L. Dueñas Carlos Jiménez-Cortegana Luis de la Cruz-Merino Antonio Pérez-Pérez Víctor Sánchez-Margalet |
| author_sort | Malika Tami |
| collection | DOAJ |
| description | Gestational diabetes mellitus (GDM) is the most common complication of pregnancy and significantly increases both maternal and fetal morbidity and mortality. Inflammation is a hallmark of GDM, and placental inflammation may play a key role in the pathophysiology of the disease. Myeloid-derived suppressor cells (MDSCs), which are innate immunosuppressive, are thought to contribute to feto-maternal tolerance. In normal pregnancies, elevated levels of MDSCs have been observed in both peripheral and umbilical cord blood. Our hypothesis postulates that trophoblasts from placentas belonging to women with GDM may have lower levels of MDSCs compared to trophoblasts from placentas originating from healthy pregnancies. Furthermore, since leptin is overexpressed in the placenta of GDM patients, we hypothesized that leptin might contribute to the reduction of MDSCs. To test this, we investigated the in vitro effects of leptin on MDSC levels in isolated peripheral blood leukocytes after 24 h of incubation. Our findings indicate that trophoblasts from placentas from women with GDM contain a lower percentage of MDSCs compared to trophoblasts from healthy pregnancies. In addition, in vitro studies demonstrated that leptin reduces the number of MDSCs in peripheral blood leukocytes.In conclusion, MDSCs are decreased in placentas from pregnancies with GDM, and leptin appears to reduce the number of MDSCs in leukocytes isolated in vitro. Increased leptin expression in trophoblasts from placentas of women with GDM may contribute to the lower levels of MDSCs, potentially playing a role in placental inflammation. However, further investigations are required to fully elucidate this mechanism. |
| format | Article |
| id | doaj-art-ed45be7edcc7472093a67cc6fef092b3 |
| institution | OA Journals |
| issn | 0171-2985 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Immunobiology |
| spelling | doaj-art-ed45be7edcc7472093a67cc6fef092b32025-08-20T02:03:14ZengElsevierImmunobiology0171-29852025-05-01230315289710.1016/j.imbio.2025.152897Decreased number of myeloid-derived suppressor cells in the placental trophoblast of gestational diabetes mellitus. Possible role of leptinMalika Tami0Lourdes Hontecillas-Prieto1Daniel García-Domínguez2Rocío Flores-Campos3Teresa Vilariño-García4Flora Sánchez-Jiménez5Pilar Guadix6José L. Dueñas7Carlos Jiménez-Cortegana8Luis de la Cruz-Merino9Antonio Pérez-Pérez10Víctor Sánchez-Margalet11Department of Medical Biochemistry and Molecular Biology, and Immunology, Medical, School. Virgen Macarena University Hospital, University of Seville, SpainDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical, School. Virgen Macarena University Hospital, University of Seville, Spain; Institute of Biomedicine of Seville, Virgen Macarena University Hospital, CSIC, University of Seville, Seville, SpainDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical, School. Virgen Macarena University Hospital, University of Seville, Spain; Institute of Biomedicine of Seville, Virgen Macarena University Hospital, CSIC, University of Seville, Seville, SpainDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical, School. Virgen Macarena University Hospital, University of Seville, SpainDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical, School. Virgen Macarena University Hospital, University of Seville, SpainDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical, School. Virgen Macarena University Hospital, University of Seville, SpainService of Obstetrics and Gynecology, Virgen Macarena University Hospital. Medical, School, University of Seville, SpainService of Obstetrics and Gynecology, Virgen Macarena University Hospital. Medical, School, University of Seville, SpainDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical, School. Virgen Macarena University Hospital, University of Seville, SpainInstitute of Biomedicine of Seville, Virgen Macarena University Hospital, CSIC, University of Seville, Seville, Spain; Medical Oncology Service, Department of Medicine, Medical School, Virgen Macarena, University Hospital, University of Seville, SpainDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical, School. Virgen Macarena University Hospital, University of Seville, SpainDepartment of Medical Biochemistry and Molecular Biology, and Immunology, Medical, School. Virgen Macarena University Hospital, University of Seville, Spain; Institute of Biomedicine of Seville, Virgen Macarena University Hospital, CSIC, University of Seville, Seville, Spain; Corresponding author at: Department of Medical Biochemistry and Molecular Biology, and Immunology, Medical, School Virgen Macarena University Hospital, University of Seville, Av. Dr. Fedriani 3, 41009 Seville, Spain.Gestational diabetes mellitus (GDM) is the most common complication of pregnancy and significantly increases both maternal and fetal morbidity and mortality. Inflammation is a hallmark of GDM, and placental inflammation may play a key role in the pathophysiology of the disease. Myeloid-derived suppressor cells (MDSCs), which are innate immunosuppressive, are thought to contribute to feto-maternal tolerance. In normal pregnancies, elevated levels of MDSCs have been observed in both peripheral and umbilical cord blood. Our hypothesis postulates that trophoblasts from placentas belonging to women with GDM may have lower levels of MDSCs compared to trophoblasts from placentas originating from healthy pregnancies. Furthermore, since leptin is overexpressed in the placenta of GDM patients, we hypothesized that leptin might contribute to the reduction of MDSCs. To test this, we investigated the in vitro effects of leptin on MDSC levels in isolated peripheral blood leukocytes after 24 h of incubation. Our findings indicate that trophoblasts from placentas from women with GDM contain a lower percentage of MDSCs compared to trophoblasts from healthy pregnancies. In addition, in vitro studies demonstrated that leptin reduces the number of MDSCs in peripheral blood leukocytes.In conclusion, MDSCs are decreased in placentas from pregnancies with GDM, and leptin appears to reduce the number of MDSCs in leukocytes isolated in vitro. Increased leptin expression in trophoblasts from placentas of women with GDM may contribute to the lower levels of MDSCs, potentially playing a role in placental inflammation. However, further investigations are required to fully elucidate this mechanism.http://www.sciencedirect.com/science/article/pii/S0171298525000312MDSCLeptinPlacentaGestational diabetes mellitus |
| spellingShingle | Malika Tami Lourdes Hontecillas-Prieto Daniel García-Domínguez Rocío Flores-Campos Teresa Vilariño-García Flora Sánchez-Jiménez Pilar Guadix José L. Dueñas Carlos Jiménez-Cortegana Luis de la Cruz-Merino Antonio Pérez-Pérez Víctor Sánchez-Margalet Decreased number of myeloid-derived suppressor cells in the placental trophoblast of gestational diabetes mellitus. Possible role of leptin Immunobiology MDSC Leptin Placenta Gestational diabetes mellitus |
| title | Decreased number of myeloid-derived suppressor cells in the placental trophoblast of gestational diabetes mellitus. Possible role of leptin |
| title_full | Decreased number of myeloid-derived suppressor cells in the placental trophoblast of gestational diabetes mellitus. Possible role of leptin |
| title_fullStr | Decreased number of myeloid-derived suppressor cells in the placental trophoblast of gestational diabetes mellitus. Possible role of leptin |
| title_full_unstemmed | Decreased number of myeloid-derived suppressor cells in the placental trophoblast of gestational diabetes mellitus. Possible role of leptin |
| title_short | Decreased number of myeloid-derived suppressor cells in the placental trophoblast of gestational diabetes mellitus. Possible role of leptin |
| title_sort | decreased number of myeloid derived suppressor cells in the placental trophoblast of gestational diabetes mellitus possible role of leptin |
| topic | MDSC Leptin Placenta Gestational diabetes mellitus |
| url | http://www.sciencedirect.com/science/article/pii/S0171298525000312 |
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