Evidence map›Paper›PMID 26038748›Full record

ReviewEmerging microbes & infections2014

The impact of the interferon-lambda family on the innate and adaptive immune response to viral infections.

Adrian Egli, Deanna M Santer, Daire O'Shea, D Lorne Tyrrell, Michael Houghton

Open access · goldAbstract readReview
In one paragraph

Review in Emerging microbes & infections, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
9.1field-weighted citation impact, top 1% 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

91 citing papers in PubMed, 154 citations in OpenAlex.

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  7. Mechanisms of Differential Signal Transduction by IFNLR1 Variants.bioRxiv : the preprint server for biology · 2025
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31 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 2 countries.

Adrian EgliInfection Biology, Department of Biomedicine, University Hospital of Basel , 4031 Basel, Switzerland ; Clinical Microbiology, University Hospital of Basel , 4031 Basel, Switzerland.
Deanna M SanterDepartment of Medical Microbiology and Immunology, and Li Ka Shing Institute of Virology, University of Alberta , Edmonton, Alberta T6G 2E1, Canada.
Daire O'SheaDepartment of Medical Microbiology and Immunology, and Li Ka Shing Institute of Virology, University of Alberta , Edmonton, Alberta T6G 2E1, Canada ; Division of Infectious Diseases, University of Alberta , Edmonton, Alberta T6G 2E1, Canada.
D Lorne TyrrellDepartment of Medical Microbiology and Immunology, and Li Ka Shing Institute of Virology, University of Alberta , Edmonton, Alberta T6G 2E1, Canada.
Michael HoughtonDepartment of Medical Microbiology and Immunology, and Li Ka Shing Institute of Virology, University of Alberta , Edmonton, Alberta T6G 2E1, Canada.
University of Alberta · CAUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type-III interferons (IFN-λ, IFNL) are the most recently described family of IFNs. This family of innate cytokines are increasingly being ascribed pivotal roles in host-pathogen interactions. Herein, we will review the accumulating evidence detailing the immune biology of IFNL during viral infection, and the implications of this novel information on means to advance the development of therapies and vaccines against existing and emerging pathogens. IFNLs exert antiviral effects via induction of IFN-stimulated genes. Common single nucleotide polymorphisms (SNPs) in the IFNL3, IFNL4 and the IFNL receptor α-subunit genes have been strongly associated with IFN-α-based treatment of chronic hepatitis C virus infection. The clinical impact of these SNPs may be dependent on the status of viral infection (acute or chronic) and the potential to develop viral resistance. Another important function of IFNLs is macrophage and dendritic cell polarization, which prime helper T-cell activation and proliferation. It has been demonstrated that IFNL increase Th1- and reduce Th2-cytokines. Therefore, can such SNPs affect the IFNL signaling and thereby modulate the Th1/Th2 balance during infection? In turn, this may influence the subsequent priming of cytotoxic T cells versus antibody-secreting B cells, with implications for the breadth and durability of the host response.

Indexed as

B cellshepatitis C virusimmune responseinnate immunityinterferon-lambdareceptorrespiratory virusesT cells

Identifiers

PMID26038748
PMCPMC4126180
OpenAlexW2057754334

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.