Evidence map›Paper›PMID 42461031›Full record

ArticleJournal of virology2026

RELMα establishes a permissive environment for influenza virus infection through direct effects on lung epithelial cells.

Roksana Shirazi, Sang Yong Kim, Aaron Cruz, James P Stumpff, Stefanie N Sveiven, Sumaya Alaama, Jennell Jennett, Brandon H Le, Meera G Nair, Juliet Morrison

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Roksana Shirazi *Department of Microbiology and Plant Pathology, University of California, Riverside, Riverside, California, USA.ORCID 0000-0002-3112-7827
Sang Yong Kim *Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California, USA.
Aaron Cruz *Department of Microbiology and Plant Pathology, University of California, Riverside, Riverside, California, USA.ORCID 0000-0003-1161-7586
James P StumpffDepartment of Microbiology and Plant Pathology, University of California, Riverside, Riverside, California, USA.
Stefanie N SveivenDivision of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California, USA.ORCID 0000-0001-6448-9827
Sumaya AlaamaDivision of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California, USA.ORCID 0009-0000-6079-3477
Jennell JennettDivision of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California, USA.
Brandon H LeInstitute for Integrative Genome Biology, Bioinformatics Core Facility, Department of Botany and Plant Sciences, University of California, Riverside, Riverside, California, USA.ORCID 0000-0001-8651-2186
Meera G Nair *Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California, USA.ORCID 0000-0002-1807-5161
Juliet Morrison *Department of Microbiology and Plant Pathology, University of California, Riverside, Riverside, California, USA.ORCID 0000-0001-7387-6351

Funding

RELMalpha-expressing macrophages mediate host disease tolerance in mucosal infectionR01AI153195 · NIAID · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI NAIR, MEERA GOH · 2020 to 2024
$3.5M
NIAID NIH HHS R01 AI153195NIH HHS R01AI153195
6 · The paper itself

Abstract

Beyond a physical barrier, the lung epithelium provides an essential line of defense against infectious pathogens, such as influenza A viruses (IAVs), by producing antimicrobial factors and triggering innate and adaptive immunity. On the other hand, IAV infects lung epithelial cells and manipulates their function to establish a non-protective, permissive environment. Identification of epithelial factors and pathways that can be targeted to restore optimal immunity would provide new therapeutic options against IAV. Here, we demonstrate an unexpected non-immune function for the cytokine RELMɑ in mediating a permissive environment for IAV infection through lung epithelial cell-intrinsic effects. Murine infection with IAV A/California/04/2009 (H1N1) led to significant RELMɑ secretion by IAV-infected EpCAM+ epithelial cells. Both whole-body and club cell-specific RELMɑ-deficient mice (

Indexed as

Epithelial CellsInfluenza A Virus, H1N1 SubtypeLungOrthomyxoviridae InfectionsAnimalsCell LineDogsHumansIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, KnockoutIntercellular Signaling Peptides and ProteinsRetnla protein, mouseepithelial cellsinfluenza virusRELMαRetnla

Identifiers

PMID42461031
PMCPMC13483350

What Socratic 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 Socratic graph.