Mechanisms of immune regulation by the placenta: Role of type I interferon and interferon‐stimulated genes signaling during pregnancy
Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the environment. The placenta is a key mediator of the fetal/maternal interaction by providing signals that regulate the function of the maternal...
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Published in | Immunological reviews Vol. 308; no. 1; pp. 9 - 24 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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01.07.2022
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Abstract | Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the environment. The placenta is a key mediator of the fetal/maternal interaction by providing signals that regulate the function of the maternal immune system as well as provides protective mechanisms to prevent the exposure of the fetus to dangerous signals. Bacterial and/or viral infection during pregnancy induce a unique immunological response by the placenta, and type I interferon is one of the crucial signaling pathways in the trophoblast cells. Basal expression of type I interferon‐β and downstream ISGs harbors physiological functions to maintain the homeostasis of pregnancy, more importantly, provides the placenta with the adequate awareness to respond to infections. The disruption of type I interferon signaling in the placenta will lead to pregnancy complications and can compromise fetal development. In this review, we focus the important role of placenta‐derived type I interferon and its downstream ISGs in the regulation of maternal immune homeostasis and protection against viral infection. These studies are helping us to better understand placental immunological functions and provide a new perspective for developing better approaches to protect mother and fetus during infections. |
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AbstractList | Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the environment. The placenta is a key mediator of the fetal/maternal interaction by providing signals that regulate the function of the maternal immune system as well as provides protective mechanisms to prevent the exposure of the fetus to dangerous signals. Bacterial and/or viral infection during pregnancy induce a unique immunological response by the placenta, and type I interferon is one of the crucial signaling pathways in the trophoblast cells. Basal expression of type I interferon‐β and downstream ISGs harbors physiological functions to maintain the homeostasis of pregnancy, more importantly, provides the placenta with the adequate awareness to respond to infections. The disruption of type I interferon signaling in the placenta will lead to pregnancy complications and can compromise fetal development. In this review, we focus the important role of placenta‐derived type I interferon and its downstream ISGs in the regulation of maternal immune homeostasis and protection against viral infection. These studies are helping us to better understand placental immunological functions and provide a new perspective for developing better approaches to protect mother and fetus during infections. Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the environment. The placenta is a key mediator of the fetal/maternal interaction by providing signals that regulate the function of the maternal immune system as well as provides protective mechanisms to prevent the exposure of the fetus to dangerous signals. Bacterial and/or viral infection during pregnancy induce a unique immunological response by the placenta, and type I interferon is one of the crucial signaling pathways in the trophoblast cells. Basal expression of type I interferon-β and downstream ISGs harbors physiological functions to maintain the homeostasis of pregnancy, more importantly, provides the placenta with the adequate awareness to respond to infections. The disruption of type I interferon signaling in the placenta will lead to pregnancy complications and can compromise fetal development. In this review, we focus the important role of placenta-derived type I interferon and its downstream ISGs in the regulation of maternal immune homeostasis and protection against viral infection. These studies are helping us to better understand placental immunological functions and provide a new perspective for developing better approaches to protect mother and fetus during infections.Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the environment. The placenta is a key mediator of the fetal/maternal interaction by providing signals that regulate the function of the maternal immune system as well as provides protective mechanisms to prevent the exposure of the fetus to dangerous signals. Bacterial and/or viral infection during pregnancy induce a unique immunological response by the placenta, and type I interferon is one of the crucial signaling pathways in the trophoblast cells. Basal expression of type I interferon-β and downstream ISGs harbors physiological functions to maintain the homeostasis of pregnancy, more importantly, provides the placenta with the adequate awareness to respond to infections. The disruption of type I interferon signaling in the placenta will lead to pregnancy complications and can compromise fetal development. In this review, we focus the important role of placenta-derived type I interferon and its downstream ISGs in the regulation of maternal immune homeostasis and protection against viral infection. These studies are helping us to better understand placental immunological functions and provide a new perspective for developing better approaches to protect mother and fetus during infections. |
Author | Hu, Anna You, Yuan Mor, Gil Maxwell, Anthony Ding, Jiahui Liao, Aihua Adzibolosu, Nicholas |
AuthorAffiliation | 1 C.S Mott center for Human Growth and Development, Department of Obstetrics and Gynecology, Wayne State University, Detroit, MI, USA 3 Institute of Reproductive Health, Center for Reproductive Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China 2 Department of Physiology, Wayne State University, Detroit, MI, USA |
AuthorAffiliation_xml | – name: 1 C.S Mott center for Human Growth and Development, Department of Obstetrics and Gynecology, Wayne State University, Detroit, MI, USA – name: 2 Department of Physiology, Wayne State University, Detroit, MI, USA – name: 3 Institute of Reproductive Health, Center for Reproductive Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China |
Author_xml | – sequence: 1 givenname: Jiahui orcidid: 0000-0001-7747-2071 surname: Ding fullname: Ding, Jiahui organization: Wayne State University – sequence: 2 givenname: Anthony surname: Maxwell fullname: Maxwell, Anthony organization: Wayne State University – sequence: 3 givenname: Nicholas surname: Adzibolosu fullname: Adzibolosu, Nicholas organization: Wayne State University – sequence: 4 givenname: Anna surname: Hu fullname: Hu, Anna organization: Wayne State University – sequence: 5 givenname: Yuan surname: You fullname: You, Yuan organization: Wayne State University – sequence: 6 givenname: Aihua orcidid: 0000-0001-8533-8315 surname: Liao fullname: Liao, Aihua organization: Huazhong University of Science and Technology – sequence: 7 givenname: Gil orcidid: 0000-0002-5499-3912 surname: Mor fullname: Mor, Gil email: gmor@med.wayne.edu organization: Wayne State University |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35306673$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1016_j_placenta_2024_10_008 crossref_primary_10_1016_j_placenta_2025_01_004 crossref_primary_10_1128_jvi_00983_24 crossref_primary_10_1186_s12978_024_01911_0 crossref_primary_10_1055_s_0043_1778017 crossref_primary_10_3390_ijms252212135 crossref_primary_10_4163_jnh_2024_57_6_605 crossref_primary_10_1016_j_cels_2024_04_002 crossref_primary_10_1016_j_metop_2025_100350 crossref_primary_10_1016_j_biopsych_2024_04_012 crossref_primary_10_3389_fimmu_2023_1198430 crossref_primary_10_1016_j_placenta_2024_11_005 crossref_primary_10_1093_toxsci_kfae147 crossref_primary_10_1039_D4NR05338A crossref_primary_10_2174_1871530323666230606120744 crossref_primary_10_3390_cimb46060366 crossref_primary_10_1016_j_placenta_2024_05_133 crossref_primary_10_1097_MD_0000000000040611 crossref_primary_10_1016_j_placenta_2024_03_002 crossref_primary_10_23946_2500_0764_2024_9_3_98_108 crossref_primary_10_1016_j_jri_2023_104189 crossref_primary_10_1155_mi_6349687 crossref_primary_10_3389_fimmu_2024_1385762 crossref_primary_10_1016_j_xcrm_2025_101974 crossref_primary_10_3390_diseases12030059 crossref_primary_10_1016_j_isci_2023_106287 crossref_primary_10_1038_s41467_024_48492_x crossref_primary_10_1073_pnas_2318176121 crossref_primary_10_1016_j_humimm_2025_111264 crossref_primary_10_4049_jimmunol_2300081 crossref_primary_10_1038_s41588_023_01399_7 crossref_primary_10_1111_imr_13102 crossref_primary_10_1262_jrd_2022_061 crossref_primary_10_1038_s41598_024_81097_4 crossref_primary_10_1016_j_ecoenv_2022_114288 crossref_primary_10_1016_j_theriogenology_2022_11_019 crossref_primary_10_1016_j_jri_2024_104235 crossref_primary_10_1016_j_virol_2024_110245 crossref_primary_10_1016_j_placenta_2024_07_315 crossref_primary_10_1136_gocm_2024_000011 |
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Keywords | type I interferon placenta interferon-stimulated genes ISG trophoblast pregnancy |
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Notes | This article is part of a series of reviews covering Immunity at the Maternal/Fetal interface appearing in Volume 308 of Immunological Reviews. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 AUTHOR CONTRIBUTIONS JD and GM wrote the document and prepared the figures. AM, NA, AH, YY and AL edited and discussed the document. |
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Snippet | Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the... |
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SubjectTerms | Antiviral Agents Developmental stages Female Fetus Fetuses Homeostasis Humans Immune response Immune system Immunity, Innate Immunology Immunoregulation Interferon Interferon Type I interferon‐stimulated genes ISG Placenta Pregnancy Pregnancy complications Signal Transduction Signaling trophoblast type I interferon Viral infections |
Title | Mechanisms of immune regulation by the placenta: Role of type I interferon and interferon‐stimulated genes signaling during pregnancy |
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