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HLA-G: An Important Mediator of Maternal-Fetal Immune-Tolerance
by
Zhuang, Baimei
, Shang, Jin
, Yao, Yuanqing
in
Animals
/ Antigens
/ Autoimmune diseases
/ CD4 antigen
/ CD8 antigen
/ Dendritic cells
/ DNA methylation
/ Embryos
/ Female
/ Fetus - immunology
/ Fetuses
/ Genes
/ Graft rejection
/ Histocompatibility antigen HLA
/ HLA-G
/ HLA-G Antigens - immunology
/ Homeostasis
/ Humans
/ Immune Privilege - immunology
/ Immunoglobulins
/ Immunological tolerance
/ Immunology
/ KIR receptor
/ Leukocyte migration
/ Lymphocytes T
/ Macrophages
/ maternal-fetal immune-tolerance
/ Microenvironments
/ Natural killer cells
/ Pregnancy
/ Proteins
/ reproductive immunology
/ Transcription factors
/ Tumor cells
/ Tumor necrosis factor-TNF
/ Tumors
2021
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HLA-G: An Important Mediator of Maternal-Fetal Immune-Tolerance
by
Zhuang, Baimei
, Shang, Jin
, Yao, Yuanqing
in
Animals
/ Antigens
/ Autoimmune diseases
/ CD4 antigen
/ CD8 antigen
/ Dendritic cells
/ DNA methylation
/ Embryos
/ Female
/ Fetus - immunology
/ Fetuses
/ Genes
/ Graft rejection
/ Histocompatibility antigen HLA
/ HLA-G
/ HLA-G Antigens - immunology
/ Homeostasis
/ Humans
/ Immune Privilege - immunology
/ Immunoglobulins
/ Immunological tolerance
/ Immunology
/ KIR receptor
/ Leukocyte migration
/ Lymphocytes T
/ Macrophages
/ maternal-fetal immune-tolerance
/ Microenvironments
/ Natural killer cells
/ Pregnancy
/ Proteins
/ reproductive immunology
/ Transcription factors
/ Tumor cells
/ Tumor necrosis factor-TNF
/ Tumors
2021
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Do you wish to request the book?
HLA-G: An Important Mediator of Maternal-Fetal Immune-Tolerance
by
Zhuang, Baimei
, Shang, Jin
, Yao, Yuanqing
in
Animals
/ Antigens
/ Autoimmune diseases
/ CD4 antigen
/ CD8 antigen
/ Dendritic cells
/ DNA methylation
/ Embryos
/ Female
/ Fetus - immunology
/ Fetuses
/ Genes
/ Graft rejection
/ Histocompatibility antigen HLA
/ HLA-G
/ HLA-G Antigens - immunology
/ Homeostasis
/ Humans
/ Immune Privilege - immunology
/ Immunoglobulins
/ Immunological tolerance
/ Immunology
/ KIR receptor
/ Leukocyte migration
/ Lymphocytes T
/ Macrophages
/ maternal-fetal immune-tolerance
/ Microenvironments
/ Natural killer cells
/ Pregnancy
/ Proteins
/ reproductive immunology
/ Transcription factors
/ Tumor cells
/ Tumor necrosis factor-TNF
/ Tumors
2021
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HLA-G: An Important Mediator of Maternal-Fetal Immune-Tolerance
Journal Article
HLA-G: An Important Mediator of Maternal-Fetal Immune-Tolerance
2021
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Overview
Maternal-fetal immune-tolerance occurs throughout the whole gestational trimester, thus a mother can accept a genetically distinct fetus without immunological aggressive behavior. HLA-G, one of the non-classical HLA class I molecules, is restricted-expression at extravillous trophoblast. It can concordantly interact with various kinds of receptors mounted on maternally immune cells residing in the uterus (e.g. CD4+ T cells, CD8+ T cells, natural killer cells, macrophages, and dendritic cells) for maintaining immune homeostasis of the maternal-fetus interface. HLA-G is widely regarded as the pivotal protective factor for successful pregnancies. In the past 20 years, researches associated with HLA-G have been continually published. Indeed, HLA-G plays a mysterious role in the mechanism of maternal-fetal immune-tolerance. It can also be ectopically expressed on tumor cells, infected sites and other pathologic microenvironments to confer a significant local tolerance. Understanding the characteristics of HLA-G in immunologic tolerance is not only beneficial for pathological pregnancy, but also helpful to the therapy of other immune-related diseases, such as organ transplant rejection, tumor migration, and autoimmune disease. In this review, we describe the biological properties of HLA-G, then summarize our understanding of the mechanisms of fetomaternal immunologic tolerance and the difference from transplant tolerance. Furthermore, we will discuss how HLA-G contributes to the tolerogenic microenvironment during pregnancy. Finally, we hope to find some new aspects of HLA-G in fundamental research or clinical application for the future.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject
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