ReviewmBio2025
Interferons in human inborn errors of disease.
Review in mBio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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
2 citing papers in PubMed.
- Ligation of the CD163 molecule inhibits the synthesis of type I and type III interferons in porcine alveolar macrophages.BMC veterinary research · 2026Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Interferons are ubiquitously produced cytokines with diverse cellular functions. IFNs play essential functions in responding to viral infections and tumorigenesis by initiating an interferon-stimulated gene response and triggering the adaptive immune response. However, excessive, prolonged IFN production disrupts cellular homeostasis and can lead to an array of severe inflammatory conditions. Due to developments in whole genome sequencing and elucidation of key signaling pathways, excessive IFN production and its associated interferon-stimulated gene expression signature is now an established molecular diagnostic of Mendelian inborn errors in immunity termed "interferonopathies." In addition, identification of Mendelian loss-of-function mutations in critical mediators of the IFN response has been identified as the causal factors of immune deficiencies and susceptibility to viral infections. Thus, IFNs and their preceding signaling pathways now represent major therapeutic targets. In this review, we outline the existing evidence on the role IFNs play in human disease and the genetic mechanisms that underlie excessive IFN production or immune deficiencies.
Indexed as
Identifiers
What OpenQuestion holds
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.