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Trophoblast-derived miR-410-5p induces M2 macrophage polarization and mediates immunotolerance at the fetal-maternal interface by targeting the STAT1 signaling pathway
Journal of Translational Medicine Open Access 04 January 2024
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References
Wang, S. C. et al. The appropriate frequency and function of decidual Tim-3(+)CTLA-4(+)CD8(+) T cells are important in maintaining normal pregnancy. Cell Death Dis. 10, 407 (2019).
Li, Y. H. et al. The Galectin-9/Tim-3 pathway is involved in the regulation of NK cell function at the maternal-fetal interface in early pregnancy. Cell. Mol. Immunol. 13, 73–81 (2016).
Okuyama, M. et al. Elevated soluble PD-L1 in pregnant women’s serum suppresses the immune reaction. Front. Immunol. 10, 86 (2019).
Wang, S. C. et al. PD-1 and Tim-3 pathways are associated with regulatory CD8(+) T-cell function in decidua and maintenance of normal pregnancy. Cell Death Dis. 6, e1738 (2015).
Lindau, R. et al. Interleukin-34 is present at the fetal-maternal interface and induces immunoregulatory macrophages of a decidual phenotype in vitro. Hum. Reprod. 33, 588–599 (2018).
Liu, J. et al. Human placental trophoblast cells contribute to maternal-fetal tolerance through expressing IL-35 and mediating iT(R)35 conversion. Nat. Commun. 10, 4601 (2019).
Meng, Y. H. et al. RANKL-mediated harmonious dialogue between fetus and mother guarantees smooth gestation by inducing decidual M2 macrophage polarization. Cell Death Dis. 8, e3105 (2017).
Vento-Tormo, R. et al. Single-cell reconstruction of the early maternal-fetal interface in humans. Nature 563, 347 (2018).
Wang, X. -Q. et al. Trophoblast-derived CXCL16 induces M2 macrophage polarization that in turn inactivates NK cells at the maternal-fetal interface. Cell. Mol. Immunol. 15, 1038–1046 (2018).
Salvany-Celades, M. et al. Three types of functional regulatory T cells control T cell responses at the human maternal-fetal interface. Cell Rep. 27, 2537 (2019).
Tilburgs, T. et al. Human HLA-G plus extravillous trophoblasts: Immune-activating cells that interact with decidual leukocytes. Proc. Natl Acad. Sci. USA 112, 7219–7224 (2015).
Poloski, E. et al. JEG-3 trophoblast cells producing human chorionic gonadotropin promote conversion of human CD4(+)FOXP3(-) T cells into CD4(+) FOXP3(+) regulatory T cells and foster T cell suppressive activity. Biol. Reprod. 94, 106 (2016).
Ban, Y. L. et al. Effect of indoleamine 2,3-dioxygenase expressed in HTR-8/SVneo cells on decidual NK cell cytotoxicity. Am. J. Reprod. Immunol. 75, 519–528 (2016).
Paparini, D. E. et al. Vasoactive intestinal peptide shapes first-trimester placenta trophoblast, vascular, and immune cell cooperation. Br. J. Pharmacol. 176, 964–980 (2019).
Kovacs, A. F. et al. Unravelling the role of trophoblastic-derived extracellular vesicles in regulatory T cell differentiation. Int. J. Mol. Sci. 20, 3457 (2019).
Acknowledgements
This work was supported by grant number MOST 2017YFC1001400 awarded to D.-J.L.; grants from the National Natural Science Foundation of China, numbers 81971456 and 81200425 awarded to X.-Q.W.; and grants from the National Natural Science Foundation of China, numbers 81471548 and 81490744 awarded to D.-J.L.
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Wang, XQ., Li, DJ. The mechanisms by which trophoblast-derived molecules induce maternal–fetal immune tolerance. Cell Mol Immunol 17, 1204–1207 (2020). https://doi.org/10.1038/s41423-020-0460-5
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DOI: https://doi.org/10.1038/s41423-020-0460-5