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The immune checkpoint molecule, VTCN1/B7-H4, guides differentiation and suppresses proinflammatory responses and MHC class I expression in an embryonic stem cell-derived model of human trophoblast.
- Source :
-
Frontiers in endocrinology [Front Endocrinol (Lausanne)] 2023 Mar 16; Vol. 14, pp. 1069395. Date of Electronic Publication: 2023 Mar 16 (Print Publication: 2023). - Publication Year :
- 2023
-
Abstract
- The placenta acts as a protective barrier to pathogens and other harmful substances present in the maternal circulation throughout pregnancy. Disruption of placental development can lead to complications of pregnancy such as preeclampsia, intrauterine growth retardation and preterm birth. In previous work, we have shown that expression of the immune checkpoint regulator, B7-H4/VTCN1, is increased upon differentiation of human embryonic stem cells (hESC) to an in vitro model of primitive trophoblast (TB), that VTCN1/B7-H4 is expressed in first trimester but not term human placenta and that primitive trophoblast may be uniquely susceptible to certain pathogens. Here we report on the role of VTCN1 in trophoblast lineage development and anti-viral responses and the effects of changes in these processes on major histocompatibility complex (MHC) class I expression and peripheral NK cell phenotypes.<br />Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.<br /> (Copyright © 2023 Zhou, Tian, Qu, Williams, Yuan, Karvas, Sheridan, Schulz, Ezashi, Roberts and Schust.)
- Subjects :
- Infant, Newborn
Pregnancy
Humans
Female
Placenta metabolism
Immune Checkpoint Proteins metabolism
Histocompatibility Antigens Class I genetics
Histocompatibility Antigens Class I metabolism
HLA Antigens
Embryonic Stem Cells
Cell Differentiation
V-Set Domain-Containing T-Cell Activation Inhibitor 1 metabolism
Trophoblasts metabolism
Premature Birth metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1664-2392
- Volume :
- 14
- Database :
- MEDLINE
- Journal :
- Frontiers in endocrinology
- Publication Type :
- Academic Journal
- Accession number :
- 37008954
- Full Text :
- https://doi.org/10.3389/fendo.2023.1069395