ArticleNature immunology2025
Tonic type I interferon signaling optimizes the antiviral function of plasmacytoid dendritic cells.
Article in Nature immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Single-cell heterogeneity in interferon induction potential is heritable and governed by variation in cell state.Cell systems · 2026Article
- Plasmacytoid Dendritic Cells Exhibit High Transferrin Receptor Expression Without Iron Accumulation.European journal of immunology · 2026Article
- Age- and tissue-dependent diversity of human plasmacytoid dendritic cells uncovers a cycling subset dominant in early life and cancer.Immunity · 2026Article
- Chromatin-mediated anticipatory control of type I interferon production in plasmacytoid dendritic cells.Immunity · 2026Article
- Commentary: The plasmacytoid dendritic cell paradox in cancer: impaired type I interferon responses in a nucleic acid-rich tumor microenvironment.Frontiers in immunology · 2026Article
- Article
- Single-cell heterogeneity in interferon induction potential is heritable and governed by variation in cell state.bioRxiv : the preprint server for biology · 2025Article
- Bridging pDCs and cDCs: The Identity of Transitional Dendritic Cells.Immunological reviews · 2025Review
Corrections and comments
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Authors and funding
25 authors.
Funding
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 'IFN-I-primed' subsets (pDC-B/C) that showed lower IFN-I responses and poor survival, but did not support virus replication. Thus, tonic IFN-I signaling decreases the cytokine-producing capacity and survival of pDCs but increases their virus resistance, facilitating optimal antiviral responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.