{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yu J"],"funding":["NCI NIH HHS"],"pagination":["4713-4732.e19"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11344674"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["187(17)"],"pubmed_abstract":["Immune tolerance mechanisms are shared in cancer and pregnancy. Through cross-analyzing single-cell RNA-sequencing data from multiple human cancer types and the maternal-fetal interface, we found B7-H4 (VTCN1) is an onco-fetal immune tolerance checkpoint. We showed that genetic deficiency of B7-H4 resulted in immune activation and fetal resorption in allogeneic pregnancy models. Analogously, B7-H4 contributed to MPA/DMBA-induced breast cancer progression, accompanied by CD8<sup>+</sup> T cell exhaustion. Female hormone screening revealed that progesterone stimulated B7-H4 expression in placental and breast cancer cells. Mechanistically, progesterone receptor (PR) bound to a newly identified -58 kb enhancer, thereby mediating B7-H4 transcription via the PR-P300-BRD4 axis. PR antagonist or B"],"journal":["Cell"],"pubmed_title":["Progestogen-driven B7-H4 contributes to onco-fetal immune tolerance."],"pmcid":["PMC11344674"],"funding_grant_id":["R01 CA152470","R01 CA248430","R01 CA193136","P30 CA046592","R01 CA123088","R01 CA099985","R01 CA261985"],"pubmed_authors":["Freeman ZT","Schon S","Lin X","Yu J","Vatan L","Grove S","Zhai Y","Skala S","Wang S","Wei S","Wicha M","Wang W","Liao P","Parolia A","Zhou J","Wen F","Zou W","Kryczek I","Szumilo J","Chen L","Yan Y","Xiao R","Chinnaiyan AM","Li X","Rizvi S","Li S","Hu J","Okla K","Lin H","Cho KR","Kotarski J","Xu Y"],"additional_accession":[]},"is_claimable":false,"name":"Progestogen-driven B7-H4 contributes to onco-fetal immune tolerance.","description":"Immune tolerance mechanisms are shared in cancer and pregnancy. Through cross-analyzing single-cell RNA-sequencing data from multiple human cancer types and the maternal-fetal interface, we found B7-H4 (VTCN1) is an onco-fetal immune tolerance checkpoint. We showed that genetic deficiency of B7-H4 resulted in immune activation and fetal resorption in allogeneic pregnancy models. Analogously, B7-H4 contributed to MPA/DMBA-induced breast cancer progression, accompanied by CD8<sup>+</sup> T cell exhaustion. Female hormone screening revealed that progesterone stimulated B7-H4 expression in placental and breast cancer cells. Mechanistically, progesterone receptor (PR) bound to a newly identified -58 kb enhancer, thereby mediating B7-H4 transcription via the PR-P300-BRD4 axis. PR antagonist or B","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2026-05-29T17:17:37.901Z","creation":"2026-04-08T05:26:20.089Z"},"accession":"S-EPMC11344674","cross_references":{"pubmed":["38968937"],"doi":["10.1016/j.cell.2024.06.012"]}}