ArticlePLoS pathogens2016
STING-Licensed Macrophages Prime Type I IFN Production by Plasmacytoid Dendritic Cells in the Bone Marrow during Severe Plasmodium yoelii Malaria.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- The impact of innate immunity on malaria parasite infection dynamics in rodent models.Frontiers in immunology · 2023Pooled it
- Emerging Role of Splenic Macrophage in Malaria Pathogenesis and Immunity.Immunity, inflammation and disease · 2025Review
- Development of clinical immunity to Plasmodium vivax following repeat controlled human malaria infection.Nature communications · 2025Article
- Exploring CD169Vaccines · 2025Review
- A protective role for type I interferon signaling following infection with Mycobacterium tuberculosis carrying the rifampicin drug resistance-conferring RpoB mutation H445Y.PLoS pathogens · 2024Article
- scRNA-seq reveals elevated interferon responses and TNF-α signaling via NFkB in monocytes in children with uncomplicated malaria.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Cytolytic circumsporozoite-specific memory CD4Nature communications · 2023Article
- A systematic analysis of the human immune response to Plasmodium vivax.The Journal of clinical investigation · 2023Article
- TLR7 modulates extramedullary splenic erythropoiesis in P. yoelii NSM-infected mice through the regulation of iron metabolism of macrophages with IFN-γ.Frontiers in immunology · 2023Article
- cGAS-STING signaling pathway in intestinal homeostasis and diseases.Frontiers in immunology · 2023Review
- Function and regulation of cGAS-STING signaling in infectious diseases.Frontiers in immunology · 2023Review
- CD169eLife · 2022Article
- Activation of cGAS-STING by Lethal Malaria N67C Dictates Immunity and Mortality through Induction of CD11bAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Temporally Evolving and Context-Dependent Functions of Cytokines That Regulate Murine Anti-Pathogens (Basel, Switzerland) · 2022Review
- Comparative transcriptomic analysis reveals translationally relevant processes in mouse models of malaria.eLife · 2022Article
- Immunosuppression in Malaria: DoPathogens (Basel, Switzerland) · 2021Review
- Tissue-resident macrophages promote early dissemination of multiple myeloma via IL-6 and TNFα.Blood advances · 2021Article
- Inducible mechanisms of disease tolerance provide an alternative strategy of acquired immunity to malaria.eLife · 2021Article
- Mapping immune variation andeLife · 2021Article
- Plasma cell dynamics in the bone marrow niche.Cell reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Malaria remains a global health burden causing significant morbidity, yet the mechanisms underlying disease outcomes and protection are poorly understood. Herein, we analyzed the peripheral blood of a unique cohort of Malawian children with severe malaria, and performed a comprehensive overview of blood leukocytes and inflammatory mediators present in these patients. We reveal robust immune cell activation, notably of CD14+ inflammatory monocytes, NK cells and plasmacytoid dendritic cells (pDCs) that is associated with very high inflammation. Using the Plasmodium yoelii 17X YM surrogate mouse model of lethal malaria, we report a comparable pattern of immune cell activation and inflammation and found that type I IFN represents a key checkpoint for disease outcomes. Compared to wild type mice, mice lacking the type I interferon (IFN) receptor exhibited a significant decrease in immune cell activation and inflammatory response, ultimately surviving the infection. We demonstrate that pDCs were the major producers of systemic type I IFN in the bone marrow and the blood of infected mice, via TLR7/MyD88-mediated recognition of Plasmodium parasites. This robust type I IFN production required priming of pDCs by CD169+ macrophages undergoing activation upon STING-mediated sensing of parasites in the bone marrow. pDCs and macrophages displayed prolonged interactions in this compartment in infected mice as visualized by intravital microscopy. Altogether our findings describe a novel mechanism of pDC activation in vivo and precise stepwise cell/cell interactions taking place during severe malaria that contribute to immune cell activation and inflammation, and subsequent disease outcomes.
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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.