{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pucella JN"],"funding":["Deutsche Forschungsgemeinschaft","Deutsche Forschungsgemeinschaft (German Research Foundation)","NIAID NIH HHS","NHLBI NIH HHS","NCI NIH HHS","U.S. Department of Health & Human Services | National Institutes of Health (NIH)","U.S. Department of Health & Human Services | National Institutes of Health"],"pagination":["1946-1961"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12662804"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(11)"],"pubmed_abstract":["Plasmacytoid dendritic cells (pDCs) mount powerful antiviral type I interferon (IFN-I) responses, yet only a fraction of pDCs produces high levels of IFN-I. Here we report that peripheral pDCs in naive mice comprise three subsets (termed A, B and C) that represent progressive differentiation stages. This heterogeneity was generated by tonic IFN-I signaling elicited in part by the cGAS/STING and TLR9 DNA-sensing pathways. A small 'IFN-I-naive' subset (pDC-A) could give rise to other subsets; it was expanded in STING deficiency or after the IFN-I receptor blockade, but was abolished by exogenous IFN-I. In response to RNA viruses, pDC-A showed increased Bcl2-dependent survival and superior IFN-I responses, but was susceptible to virus infection. Conversely, the majority of pDCs comprised the "],"journal":["Nature immunology"],"pubmed_title":["Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells."],"pmcid":["PMC12662804"],"funding_grant_id":["AI158808","AI128949","R01 AI072571","U19 AI128949","HL145997","EI1185/1-1","F32 HL145997","R37 AI072571","T32 CA009161","P30 CA016087","AI072571","CA009161","F32 CA232666","R01 AI158808","CA232666"],"pubmed_authors":["Perez OA","Bandeira Sulczewski F","Eichinger A","Ivanova E","Esteva E","Smibert P","Stoeckius M","Reizis B","Dolgalev I","Ra AC","Cadwell K","Ni H","Pucella JN","Sota S","Soni C","Idoyaga J","Weisberg SP","Feng J","Das A","Stetson DB","Zhong J","Maqueda-Alfaro RA","Khodadadi-Jamayran A","Farber DL","Koralov SB"],"additional_accession":[]},"is_claimable":false,"name":"Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells.","description":"Plasmacytoid dendritic cells (pDCs) mount powerful antiviral type I interferon (IFN-I) responses, yet only a fraction of pDCs produces high levels of IFN-I. Here we report that peripheral pDCs in naive mice comprise three subsets (termed A, B and C) that represent progressive differentiation stages. This heterogeneity was generated by tonic IFN-I signaling elicited in part by the cGAS/STING and TLR9 DNA-sensing pathways. A small 'IFN-I-naive' subset (pDC-A) could give rise to other subsets; it was expanded in STING deficiency or after the IFN-I receptor blockade, but was abolished by exogenous IFN-I. In response to RNA viruses, pDC-A showed increased Bcl2-dependent survival and superior IFN-I responses, but was susceptible to virus infection. Conversely, the majority of pDCs comprised the ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-05T21:43:21.083Z","creation":"2026-05-22T03:15:52.747Z"},"accession":"S-EPMC12662804","cross_references":{"pubmed":["41087726"],"doi":["10.1038/s41590-025-02279-4"]}}