Evidence map›Paper›PMID 42218198›Full record

ArticleScientific reports2026

Dupilumab attenuate IL-4 and IL-13 synergistic effect on airway remodeling in asthma via blocking IL-4Rα/STAT6 axis.

Lina Sahnoon, Rola Abujabal, Tasneem M Alanta, Bushra Mdkhana, Ronald Olivenstein, Ellen Puré, Bassam Mahboub, Yves Laumonnier, Rifat Hamoudi, Khuloud Bajbouj and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

11 authors.

Lina SahnoonResearch Institute of Medical and Health Sciences, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates.
Rola AbujabalResearch Institute of Medical and Health Sciences, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates.
Tasneem M AlantaResearch Institute of Medical and Health Sciences, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates.
Bushra MdkhanaResearch Institute of Medical and Health Sciences, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates.
Ronald OlivensteinMeakins-Christie Laboratories, McGill University, Montreal, QC, Canada.
Ellen PuréDepartment of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Bassam MahboubDepartment of Pulmonary Medicine, Rashid Hospital, Dubai, United Arab Emirates. drbassam_mahboub@yahoo.com.
Yves LaumonnierInstitute for Nutritional Medicine, University of Lübeck, Lübeck, Germany.
Rifat HamoudiResearch Institute of Medical and Health Sciences, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates.
Khuloud BajboujDepartment of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA. kbajbouj@upenn.edu.
Qutayba HamidResearch Institute of Medical and Health Sciences, University of Sharjah, P.O. Box 27272, Sharjah, United Arab Emirates. qalheialy@sharjah.ac.ae.

Funding

Sanofi iEnvision tracking no. 2023ESR0000123University of Sharjah 32012
6 · The paper itself

Abstract

Airway fibrosis in severe asthma is a hallmark of disease pathology, yet the mechanisms driving fibroblast activation remain incompletely understood. While interleukin-4 (IL-4) and interleukin-13 (IL-13) are central to type 2 inflammation, their combined role in directly promoting human lung fibroblast-mediated fibrosis is not well defined. This study demonstrates that IL-4 and IL-13 act synergistically on asthmatic fibroblasts to potentiate a pro-fibrotic program via the shared interleukin-4 receptor alpha (IL-4Rα)/Signal Transducer and Activator of Transcription 6 (STAT6) axis. We found that diseased human lung fibroblasts (DHLFs) from asthmatic patients exhibited elevated expression of the type II receptor (IL-4Rα/IL-13Rα1) compared to normal human lung fibroblasts (NHLFs), priming them for activation. Consequently, combined IL-4/IL-13 stimulation synergistically enhanced STAT6 phosphorylation and robustly upregulated key extracellular matrix (ECM) components (collagen I/III, fibronectin) and regulators (matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1/2 (TIMP-1/2). Furthermore, IL-4 specifically emerged as the dominant driver of fibroblast proliferation. Critically, the IL-4Rα-blocking antibody dupilumab effectively abrogated this pro-fibrotic response. These findings provide a direct mechanistic basis for targeting the IL-4Rα pathway to mitigate airway remodeling and potentially alter the progressive course of fibrosis in patients with severe, type 2-high asthma.

Indexed as

Airway RemodelingAntibodies, Monoclonal, HumanizedAsthmaInterleukin-13Interleukin-4Interleukin-4 Receptor alpha SubunitSTAT6 Transcription FactorCells, CulturedFibroblastsHumansSignal TransductionAntibodies, Monoclonal, HumanizeddupilumabIL13 protein, humanIL4 protein, humanIL4R protein, humanInterleukin-13Interleukin-4Interleukin-4 Receptor alpha SubunitSTAT6 protein, humanSTAT6 Transcription FactorAirway remodelingAsthmaDupilumabFibrosisInterleukin-13 (IL-13)Interleukin-4 (IL-4)

Identifiers

PMID42218198
PMCPMC13458785

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.