Abstract
Pregnancy is a complex but well-arranged process, and a healthy fetus requires immune privilege and surveillance in the presence of paternally derived antigens. Maternal and fetal cells interact at the maternal–fetal interface. The upregulation and downregulation of maternal immunity executed by the leukocyte population predominantly depend on the activity of decidual natural killer cells and trophoblasts and are further modulated by a series of duplex signals. The B7 family, which consists of B7-1, B7-2, B7-H1, B7-DC, B7-H2, B7-H3, B7-H4, B7-H5, BTNL2, B7-H6, and B7-H7, is one of the most characterized and widely distributed signaling molecule superfamilies and conducts both stimulatory and inhibitory signals through separate interactions. In particular, the roles of B7-1, B7-2, B7-H1, and their corresponding receptors in the progression of normal pregnancy and some pregnancy complications have been extensively studied. Together with the TCR–MHC complex, B7 and its receptors play a critical role in cell proliferation and cytokine secretion. Depending on this ligand–receptor crosstalk, the balance between the tolerance and rejection of the fetus is perfectly maintained. This review aims to provide an overview of the current knowledge of the B7 family and its functions in regulating maternal–fetal immunity through individual interactions.
Highlights
Pregnancy is a complex but well-orchestrated process, and studies conducted in mice have indicated that the maternal immune system is exposed to paternally inherited fetal antigens as early as at the time of insemination
This review aims to provide an overview of the current knowledge of the B7 family and its functions in regulating maternal–fetal immunity through individual ligand– receptor complexes
Following Toxoplasma gondii infection, the upregulation of CD80/CD86 on decidual dendritic cells (DCs) contributes to abnormal pregnancy outcomes [28]. These findings indicate that B7-1 and B7-2 assist decidual DCs in maintaining a Th2-dominant state, which is beneficial to a gestational outcome
Summary
Pregnancy is a complex but well-orchestrated process, and studies conducted in mice have indicated that the maternal immune system is exposed to paternally inherited fetal antigens as early as at the time of insemination. Recent studies have indicated an important role for immunomodulators in facilitating maternal T-cell tolerance to fetal antigens. The B7 family is one of the most characterized cosignaling network superfamilies and plays an important role in the modification of T-cell activation and tolerance [3]. This review aims to provide an overview of the current knowledge of the B7 family and its functions in regulating maternal–fetal immunity through individual ligand– receptor complexes. It highlights the potency of the in vitro blockage of specific members of the B7 family for miscarriage immunotherapy
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