{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chrisikos TT"],"funding":["HHS | National Institutes of Health","NIAID NIH HHS","NCI NIH HHS","Cancer Prevention and Research Institute of Texas"],"pagination":["1286-1299"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9529896"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["209(7)"],"pubmed_abstract":["Type I conventional dendritic cells (cDC1s) are an essential Ag-presenting population required for generating adaptive immunity against intracellular pathogens and tumors. While the transcriptional control of cDC1 development is well understood, the mechanisms by which extracellular stimuli regulate cDC1 function remain unclear. We previously demonstrated that the cytokine-responsive transcriptional regulator STAT3 inhibits polyinosinic:polycytidylic acid [poly(I:C)]-induced cDC1 maturation and cDC1-mediated antitumor immunity in murine breast cancer, indicating an intrinsic, suppressive role for STAT3 in cDC1s. To probe transcriptional mechanisms regulating cDC1 function, we generated novel RNA sequencing datasets representing poly(I:C)-, IL-10-, and STAT3-mediated gene expression respons"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["STAT3 Inhibits Autocrine IFN Signaling in Type I Conventional Dendritic Cells."],"pmcid":["PMC9529896"],"funding_grant_id":["R01 AI133822","R01AI109294","P30 CA016672","R56 AI109294","R01AI133822","RP170067","R01 AI109294","RP210028"],"pubmed_authors":["Kahn LM","Shen L","Watowich SS","Brooks A","Patel B","Chrisikos TT","Zhou Y","Denne NL","Wang J"],"additional_accession":[]},"is_claimable":false,"name":"STAT3 Inhibits Autocrine IFN Signaling in Type I Conventional Dendritic Cells.","description":"Type I conventional dendritic cells (cDC1s) are an essential Ag-presenting population required for generating adaptive immunity against intracellular pathogens and tumors. While the transcriptional control of cDC1 development is well understood, the mechanisms by which extracellular stimuli regulate cDC1 function remain unclear. We previously demonstrated that the cytokine-responsive transcriptional regulator STAT3 inhibits polyinosinic:polycytidylic acid [poly(I:C)]-induced cDC1 maturation and cDC1-mediated antitumor immunity in murine breast cancer, indicating an intrinsic, suppressive role for STAT3 in cDC1s. To probe transcriptional mechanisms regulating cDC1 function, we generated novel RNA sequencing datasets representing poly(I:C)-, IL-10-, and STAT3-mediated gene expression respons","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2026-05-28T02:02:34.06Z","creation":"2025-04-05T15:22:46.812Z"},"accession":"S-EPMC9529896","cross_references":{"pubmed":["36038291"],"doi":["10.4049/jimmunol.2101104"]}}