ArticleNature immunology2025
TNF and type I interferon crosstalk controls the fate and 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. An erratum has been issued. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed.
- Review
- Autoimmunity and peginterferon therapy for polycythemia vera.HemaSphere · 2026Review
- Pan-cancer single-cell atlases of mouse and human tumor-associated dendritic cells.Nature communications · 2026Article
- Age- and tissue-dependent diversity of human plasmacytoid dendritic cells uncovers a cycling subset dominant in early life and cancer.Immunity · 2026Article
- Identification of Mannose-Capped-Arabinomannan 101-mer as a Potential Influenza Virus Vaccine Adjuvant.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Chemoradiation of glioblastoma cells alters expression of activation and immune checkpoint molecules on type 1 and 2 dendritic cells and impacts on subsequent T cell proliferation.Clinical and translational radiation oncology · 2026Article
- Review
- Bulk and Single-Cell Transcriptomics Reveal That SCO2 Drives Psoriasis via Activating CCR7International journal of molecular sciences · 2026Article
- Plasmacytoid dendritic cells in systemic and cutaneous lupus erythematosus: an evolving understanding.Frontiers in immunology · 2026Review
- Dysregulated expression of PSGL-1 and ADAM8 in Sjögren's disease: potential contribution to disease pathogenesis.Frontiers in immunology · 2026Article
- Immunosenescence and susceptibility to respiratory viruses: a state-of-the-art review.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Predominant lung cDC2 phenotype in cigarette smoke-exposed mice favors polarization of IL-17-producing CD4American journal of physiology. Lung cellular and molecular physiology · 2026Article
- CGRP: the immune system's double agent - context-dependent roles in inflammation, resolution and cancer.Frontiers in immunology · 2026Review
- Ontogenetic Diversification of Type 2 Conventional Dendritic Cells in the Bone Marrow: A Central Logic for Peripheral Immunity.Immunological reviews · 2025Review
- Bridging pDCs and cDCs: The Identity of Transitional Dendritic Cells.Immunological reviews · 2025Review
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
Plasmacytoid dendritic cells (pDCs) are major producers of type I interferon (IFN-I), an important antiviral cytokine, and activity of these cells must be tightly controlled to prevent harmful inflammation and autoimmunity. Evidence exists that one regulatory mechanism is a fate-switching process from an IFN-I-secreting pDC to a professional antigen-presenting conventional dendritic cell (cDC) that lacks IFN-I-secreting capacity. However, this differentiation process is controversial owing to limitations in tracking the fate of individual cells over time. Here we use single-cell omics and functional experiments to show that activated human pDCs can lose their identity as IFN-I-secreting cells and acquire the transcriptional, epigenetic and functional features of cDCs. This pDC fate-switching process is promoted by tumor necrosis factor but blocked by IFN-I. Importantly, it occurs in vivo during human skin inflammatory diseases and injury, and physiologically in elderly people. This work identifies the pDC-to-cDC reprogramming trajectory and unveils a mechanistic framework for harnessing it therapeutically.
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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.