Evidence map›Paper›PMID 41675499›Full record

ReviewFrontiers in immunology2025

Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.

Irina Lyadova

Abstract readReview
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Irina LyadovaLaboratory of Cellular and Molecular Basis of Histogenesis, Koltzov Institute of Developmental Biology of the Russian Academy of Sciences, Moscow, Russia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Bacterial InfectionsInterferon Type IMyeloid CellsAnimalsHost-Pathogen InteractionsHumansMacrophage ActivationMacrophagesSignal TransductionInterferon Type Ibacterial infectionsinflammatory hematopoiesismacrophagesneutrophilstype I interferons

Identifiers

PMID41675499
PMCPMC12886446

What OpenQuestion holds

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Registered trials

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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.