ArticleJournal of medical virology2026
IL-19 Modulates Antiviral Immunity and Inflammation via IL-20RB/STAT3/TRIM22 Signaling Pathway.
Article in Journal of medical virology, 2026. 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
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
1 citing paper in PubMed.
- IL-19 Modulates Antiviral Immunity and Inflammation via IL-20RB/STAT3/TRIM22 Signaling Pathway.Journal of medical virology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Interleukins (ILs) are pleiotropic mediators of immune signaling and represent promising targets for antiviral intervention. Among them, IL-19 is upregulated in response to viral infections, yet its functional significance and mechanistic basis have been poorly defined. This study identifies an unforeseen antiviral activity of IL-19. Mechanistically, we demonstrate that IL-19 signals through the IL-20RB receptor to drive STAT3 phosphorylation, and this activated IL-20RB/STAT3 pathway then induces TRIM22 expression, culminating in enhanced IFN-λ secretion and the direct suppression of viral replication. Importantly, despite significantly curtailing HSV-1 replication in murine brain and lung tissues, IL-19 administration failed to confer a survival benefit, an effect attributable to aggravated pulmonary inflammation. These findings clarify IL-19 as a dual-function cytokine with both protective antiviral and detrimental proinflammatory properties, illustrating the intricate immunomodulatory functions of cytokines during viral infections.
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.