ArticleThe Journal of experimental medicine2021
SARS-CoV-2 induces human plasmacytoid predendritic cell diversification via UNC93B and IRAK4.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed.
- Impaired function and delayed regeneration of dendritic cells in COVID-19.PLoS pathogens · 2021Trial
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- Observations of Wart Clearance Following COVID-19 Vaccination: Coincidence or Missed Immunologic Signals?Vaccines · 2025Article
- Type I IFNs Decrease SARS-CoV-2 Replication in Human Cardiomyocytes and Increase Cytokine Production in Macrophages.Journal of clinical immunology · 2025Article
- Differential response of human plasmacytoid pre-dendritic cells to SARS-CoV-2 variants.iScience · 2025Article
- New insights into the role of IFN-α/β and TLR7/8/9 in cancer immunotherapy and systemic autoimmunity.Journal for immunotherapy of cancer · 2025Review
- In Vitro Investigation of Statin Effects on Genes Associated with Severe COVID-19 in Cancerous and Non-Cancerous Cells.Biomedicines · 2025Article
- Enhanced TLR7-dependent production of type I interferon by pDCs underlies pandemic chilblains.The Journal of experimental medicine · 2025Article
- DOCK2 Deficiency and GATA2 Haploinsufficiency Can Underlie Critical Coronavirus Disease 2019 (COVID-19) Pneumonia.Journal of clinical immunology · 2025Article
- Sensing of SARS-CoV-2-infected cells by plasmacytoid dendritic cells is modulated via an interplay between CD54/ICAM-1 and CD11a/LFA-1 αJournal of virology · 2025Article
- SARS-CoV-2 S, M, and E Structural Glycoproteins Differentially Modulate Endoplasmic Reticulum Stress Responses.International journal of molecular sciences · 2025Article
- Human genetic and immunological determinants of SARS-CoV-2 infection and multisystem inflammatory syndrome in children.Clinical and experimental immunology · 2025Review
- Recent Advances in Our Understanding of Human Inflammatory Dendritic Cells in Human Immunodeficiency Virus Infection.Viruses · 2025Review
- Modulation of IRAK4 as a therapeutic strategy against monosodium urate- and xanthine-induced inflammation in macrophages and HepG2 cells.Frontiers in immunology · 2025Article
- Characterization of TLR9 responsiveness in cell subsets derived fromFrontiers in immunology · 2025Article
- COVID-19: from immune response to clinical intervention.Precision clinical medicine · 2024Review
- The role of plasmacytoid dendritic cells (pDCs) in immunity during viral infections and beyond.Cellular & molecular immunology · 2024Review
- The conneXion between sex and immune responses.Nature reviews. Immunology · 2024Review
- The role of dendritic cells in respiratory viral infection.European respiratory review : an official journal of the European Respiratory Society · 2024Review
39 more citing papers are in PubMed but not listed here.
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16 authors.
Funding
Abstract
Several studies have analyzed antiviral immune pathways in late-stage severe COVID-19. However, the initial steps of SARS-CoV-2 antiviral immunity are poorly understood. Here we have isolated primary SARS-CoV-2 viral strains and studied their interaction with human plasmacytoid predendritic cells (pDCs), a key player in antiviral immunity. We show that pDCs are not productively infected by SARS-CoV-2. However, they efficiently diversified into activated P1-, P2-, and P3-pDC effector subsets in response to viral stimulation. They expressed CD80, CD86, CCR7, and OX40 ligand at levels similar to influenza virus-induced activation. They rapidly produced high levels of interferon-α, interferon-λ1, IL-6, IP-10, and IL-8. All major aspects of SARS-CoV-2-induced pDC activation were inhibited by hydroxychloroquine. Mechanistically, SARS-CoV-2-induced pDC activation critically depended on IRAK4 and UNC93B1, as established using pDC from genetically deficient patients. Overall, our data indicate that human pDC are efficiently activated by SARS-CoV-2 particles and may thus contribute to type I IFN-dependent immunity against SARS-CoV-2 infection.
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