Evidence map›Paper›PMID 27617757›Full record

ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2016

Immune Cell Profiling of IFN-λ Response Shows pDCs Express Highest Level of IFN-λR1 and Are Directly Responsive via the JAK-STAT Pathway.

Aoife Kelly, Mark W Robinson, Gerard Roche, Christine A Biron, Cliona O'Farrelly, Elizabeth J Ryan

Abstract read
In one paragraph

Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
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

35 citing papers in PubMed, 49 citations in OpenAlex.

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  5. Structure-function of type I and III interferons.Current opinion in immunology · 2024
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  9. Recent advances in cutaneous lupus.Journal of autoimmunity · 2022
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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

6 authors at 3 institutions in 2 countries.

Aoife Kelly1 School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin , Dublin, Ireland .
Mark W Robinson1 School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin , Dublin, Ireland .
Gerard Roche1 School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin , Dublin, Ireland .
Christine A Biron2 Department of Molecular Microbiology and Immunology, Brown University , Providence, Rhode Island.
Cliona O'Farrelly1 School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin , Dublin, Ireland .
Elizabeth J Ryan4 Centre for Colorectal Disease, Education and Research Centre, St. Vincent's University Hospital , Dublin, Ireland .
Trinity College Dublin · IEBrown University · USSt. Vincent's University Hospital · IE

Funding

Type 1 IFN Function and Signaling in Immunity to VirusesR01AI055677 · NIAID · BROWN UNIVERSITY · PI BIRON, CHRISTINE A. · 2003 to 2013
$3.5M
NIAID NIH HHS R01 AI055677
6 · The paper itself

Abstract

The interferon lambda (IFN-λ) cytokines have well-known antiviral properties, yet their contribution to immune regulation is not well understood. Epithelial cells represent the major target cell of IFN-λ; peripheral blood mononuclear cells are generally considered nonresponsive, with the exception of plasmacytoid dendritic cells (pDCs). In this study we aimed to define the potential for discrete subpopulations of cells to directly respond to IFN-λ. Analysis of peripheral blood leukocytes reveals that, while pDCs uniformly express the highest levels of IFN-λ receptor, a small proportion of B cells and monocytes also express the receptor. Nevertheless, B cells and monocytes respond poorly to IFN-λ stimulation in vitro, with minimal STAT phosphorylation and interferon-stimulated gene (ISG) induction observed. We confirm that pDCs respond to IFN-λ in vitro, upregulating their expression of pSTAT1, pSTAT3, and pSTAT5. However, we found that pDCs do not upregulate pSTAT6 in response to IFN-λ treatment. Our results highlight unique aspects of the response to IFN-λ and confirm that while the IFN-λ receptor is expressed by a small proportion of several different circulating immune cell lineages, under normal conditions only pDCs respond to IFN-λ stimulation with robust STAT phosphorylation and ISG induction. The difference in STAT6 responsiveness of pDCs to type I and type III interferons may help explain the divergence in their biological activities.

Indexed as

Antigens, CDAntiviral AgentsB-LymphocytesDendritic CellsGene Expression RegulationHumansImmunophenotypingInterferon-alphaInterferon LambdaInterferon Regulatory FactorsInterferonsInterleukinsJanus KinasesLeukocytes, MononuclearMonocytesPhosphorylationAntigens, CDAntiviral AgentsInterferon-alphaInterferon Lambdainterferon-lambda, humanInterferon Regulatory FactorsInterferonsInterleukinsJanus KinasesReceptors, InterferonSTAT Transcription Factorsdendritic cellsJAK-STATperipheral blood mononuclear cellsType III IFNs

Identifiers

PMID27617757
PMCPMC5165669
OpenAlexW2529608238

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.