ArticleJournal of innate immunity2026
Mechanisms of Differential Signal Transduction by Interferon Lambda Receptor 1 Variants.
Article in Journal of innate immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Update of
Authors and funding
6 authors.
Funding
Abstract
introductionLambda interferons signal through the interferon lambda receptor 1 (IFNLR1) and IL10RB heterodimer to induce interferon stimulated genes (ISGs). We previously showed that proteins derived from distinct IFNLR1 splice isoforms uniquely influence gene expression and hepatitis B virus replication in stem cell-derived hepatocytes (iHeps). Here, we evaluated signal transduction mechanisms of full-length IFNLR1 (variant 1) and a truncated variant missing part of the cytoplasmic JAK1-interacting domain (variant 2).
methodsWe evaluated HEK293T cells, wild-type (WT), and IFNLR1 knockout (KO) iHeps with doxycycline-inducible expression of FLAG-tagged IFNLR1 variants using the Duolink proximity ligation assay, ImageStream flow cytometry, Western blotting, susceptibility to JAK1 and TYK2 inhibitors, and gene expression profiling.
resultsEach variant colocalized with IL10RB after IFNL3 treatment, but variant 1 was more rapidly and extensively internalized. In WT iHeps, overexpression of variant 1 or variant 2 enabled higher IFNL-induced JAK1, TYK2, STAT1, and STAT2 phosphorylation, yet variant 2 supported less robust ISG induction. In KO iHeps, variant 2 supported less JAK1 and TYK2 phosphorylation and ISG induction than variant 1, yet supported comparable STAT1 and STAT2 phosphorylation. In iHeps expressing variant 1, WT iHeps were more resistant than KO iHeps to TYK2 inhibition of antiviral ISG induction, yet were more susceptible to TYK2 inhibition of proinflammatory ISG induction, suggesting endogenous noncanonical variants influence TYK2-signaling dependence.
conclusionIFNLR1 variants promote differential utilization of signaling mediators to influence IFNL-induced gene expression patterns, indicating a putative role in pathway regulation.
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.