ReviewFrontiers in immunology2025
Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Neutrophils repurpose the nucleolus as a cytokine reservoir and secretory organelle.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferons (IFN-I) are multifunctional cytokines with well-established antiviral and antitumor activities. In viral infections and cancer, IFN-I are largely protective, acting through both direct mechanisms, such as induction of antiviral or antiproliferative programs, and indirect mechanisms, mediated through the activation of immune effector cells. During bacterial infections, IFN-I primarily act indirectly, making their role more complex and contradictory. Depending on the context, IFN-I may promote host protection or contribute to pathology, and factors determining these divergent outcomes remain poorly understood. Comparative analysis of existing studies indicates that discrepancies in IFN-I effects arise from multiple pathogen- and host-dependent factors, including pathogen biology, the route of pathogen delivery, infection stage, host immune competence, the magnitude of IFN-I response and other parameters. Among them, the ability of IFN-I to reprogram myeloid cell responses appears to be a critical but insufficiently characterized determinant. This review synthesizes current evidence on IFN-I responses in bacterial infections, with particular emphasis on their effects in the myeloid cell compartment. These include IFN-I ability to inhibit macrophage activation, alter macrophage metabolism, induce myeloid cell death, affect macrophage and neutrophil recruitment, and modulate myeloid cell generation by supporting emergency hematopoiesis and redirecting lineage output toward monocyte or granulocyte generation. Given that macrophages and neutrophils differentially contribute to protection or pathology across various bacterial infections, such effects may underlie both beneficial and detrimental outcomes of IFN-I signaling. The review highlights IFN-I-driven regulation of myeloid cell activity and myelopoiesis as overlooked checkpoints in bacterial pathogenesis, providing a framework for future mechanistic studies and guiding the search for new opportunities in therapeutic intervention.
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