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The immune checkpoint molecule, B7-H4/VTCN1, guides differentiation and suppresses proinflammatory responses and MHC class I expression in an embryonic stem cell-derived model of primitive human trophoblast I

ABSTRACT: VTCN1/B7-H4 is expressed in human embryonic stem cells (hESC) to an in vitro model of primitive trophoblast (TB) and first trimester but not term human placenta and that primitive trophoblast may be uniquely susceptible to certain pathogens.

ORGANISM(S): Homo sapiens

PROVIDER: GSE227094 | GEO | 2023/03/13

REPOSITORIES: GEO

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The immune checkpoint molecule, B7-H4/VTCN1, guides differentiation and suppresses proinflammatory responses and MHC class I expression in an embryonic stem cell-derived model of primitive human trophoblast III

Project description:VTCN1/B7-H4 is expressed in human embryonic stem cells (hESC) to an in vitro model of primitive trophoblast (TB) and first trimester but not term human placenta and that primitive trophoblast may be uniquely susceptible to certain pathogens.

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Pancreatic epithelial IL-17/IL-17RA signaling drives B7-H4 to promote tumorigenesis

Project description:IL-17 is required for the initiation and progression of pancreatic cancer, particularly in the context of inflammation, as previously shown by genetic and pharmacological approaches. The cellular compartment and downstream molecular mediators of IL-17-mediated pancreatic tumorigenesis have not been fully identified. We interrogated the cellular compartment required by generating transgenic animals with Interleukin 17 receptor A (IL-17RA) genetically deleted from the pancreatic epithelial compartment vs. the hematopoietic compartment via generation of IL-17RA-deficient (IL17-RA-/-) bone marrow chimeras, in the context of embryonically activated or inducible Kras. Deletion of IL-17RA from the pancreatic epithelial compartment, but not from hematopoietic, resulted in delayed premalignant lesions initiation and progression and increased CD8+ cytotoxic T cells infiltration to the tumor microenvironment. Absence of IL-17RA in the pancreatic compartment affected transcriptional profiles of epithelial cells, modulating stemness and immunological pathways. Interestingly, B7-H4, a known inhibitor of T cell activation encoded by the gene Vtcn1, was the most upregulated checkpoint molecule via IL17 early during pancreatic tumorigenesis, and its genetic deletion delayed pancreatic premalignant lesions development and reduced immunosuppression. We reveal pancreatic epithelial IL-17RA requirement for pancreatic tumorigenesis by reprogramming the immune pancreatic landscape which is partially orchestrated by regulation of B7-H4.

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Project description:The goal of this study are to find the abonormally expressed genes of B7-H4-/- leukemia inital cells in MLL-AF9 induced AML mice by RNA-seq analysis.Methods: Lin- festival liver cells were isolated from WT and B7-H4-null mice and infected with MLL-AF9 retroviruses, then transplanted to the lethally irradiated recipient mice. When AML developed, we isolated the YFP+/Mac-1+/c-Kit+ bone marrow cells by FACS and and then made the RNA-sequence using Illumina. Results: We identified 27180 transcripts in wild type and B7-H4-/- leukemia initial cells. 572 transcripts showed differential expression between the WT and B7-H4−/− LICs, with a fold change ≥1.5 and p value <0.01. 271 transcripts were downregulated and 241 transcripts were upregulated.

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