Evidence map›Paper›PMID 27298374›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

OX40L blockade protects against inflammation-driven fibrosis.

Muriel Elhai, Jérôme Avouac, Anna Maria Hoffmann-Vold, Nadira Ruzehaji, Olivia Amiar, Barbara Ruiz, Hassina Brahiti, Matthieu Ponsoye, Maxime Fréchet, Anne Burgevin and 12 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
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  4. Regulatory T Cell-Based Adoptive Cell Therapy in Autoimmunity.International journal of molecular sciences · 2025
    Review
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  9. Human OX40L-CAR-TScience translational medicine · 2024
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 9 institutions in 4 countries.

Muriel ElhaiINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France; Rheumatology A Department, Cochin Hospital, Paris Descartes University, 75014 Paris, France;
Jérôme AvouacINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France; Rheumatology A Department, Cochin Hospital, Paris Descartes University, 75014 Paris, France;
Anna Maria Hoffmann-VoldDepartment of Rheumatology, Oslo University Hospital, 0873 Oslo, Norway;
Nadira RuzehajiINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France;
Olivia AmiarINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France;
Barbara RuizINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France;
Hassina BrahitiINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France;
Matthieu PonsoyeINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France;
Maxime FréchetINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France;
Anne BurgevinINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France;
Sonia PezetINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France;
Jérémy SadoineEquipe d'Accueil (EA) 2496 Pathologie, Imagerie et Biothérapies Orofaciales, Faculty of Odontology, Paris Descartes University, Sorbonne Paris Cite, 92120 Montrouge, France; Plateforme d'Imagerie Du Vivant, Le Pôle de Recherche et d'Enseignement Supérieur Sorbonne Paris Cité, 92120 Montrouge, France;
Thomas GuilbertINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France;
Carole NiccoINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France;
Hisaya AkibaDepartment of Immunology, Juntendo University School of Medicine, Tokyo 113-8421, Japan;
Vigo HeissmeyerResearch Unit Molecular Immune Regulation, Institute of Molecular Immunology, Helmholtz Zentrum München, DE-81377 Munich, Germany; Institute for Immunology, Ludwig-Maximilians-Universität München, DE-80336 Munich, Germany;
Arun SubramaniamImmune Mediated Diseases, Sanofi Genzyme, Framingham, MA 01701;
Robert ResnickImmune Mediated Diseases, Sanofi Genzyme, Framingham, MA 01701;
Øyvind MolbergDepartment of Rheumatology, Oslo University Hospital, 0873 Oslo, Norway;
André KahanRheumatology A Department, Cochin Hospital, Paris Descartes University, 75014 Paris, France;
Gilles ChiocchiaINSERM, U1173, Faculty of Health Sciences Simone Veil, Université Versailles-Saint-Quentin, 78180 Saint-Quentin-En-Yvelines, France.
Yannick AllanoreINSERM, U1016 UMR8104, Cochin Institute, Paris Descartes University, Sorbonne Paris Cite, 75014 Paris, France; Rheumatology A Department, Cochin Hospital, Paris Descartes University, 75014 Paris, France; yannick.allanore@cch.aphp.fr.
Université Paris Cité · FRDélégation Paris 5 · FRInserm · FROslo University Hospital · NOSorbonne Paris Cité · FRHôpital Cochin · FRJuntendo University · JPLudwig-Maximilians-Universität München · DEUniversité de Versailles Saint-Quentin-en-Yvelines · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treatment for fibrosis represents a critical unmet need, because fibrosis is the leading cause of death in industrialized countries, and there is no effective therapy to counteract the fibrotic process. The development of fibrosis relates to the interplay between vessel injury, immune cell activation, and fibroblast stimulation, which can occur in various tissues. Immunotherapies have provided a breakthrough in the treatment of immune diseases. The glycoprotein OX40-OX40 ligand (OX40L) axis offers the advantage of a targeted approach to costimulatory signals with limited impact on the whole immune response. Using systemic sclerosis (SSc) as a prototypic disease, we report compelling evidence that blockade of OX40L is a promising strategy for the treatment of inflammation-driven fibrosis. OX40L is overexpressed in the fibrotic skin and serum of patients with SSc, particularly in patients with diffuse cutaneous forms. Soluble OX40L was identified as a promising serum biomarker to predict the worsening of lung and skin fibrosis, highlighting the role of this pathway in fibrosis. In vivo, OX40L blockade prevents inflammation-driven skin, lung, and vessel fibrosis and induces the regression of established dermal fibrosis in different complementary mouse models. OX40L exerts potent profibrotic effects by promoting the infiltration of inflammatory cells into lesional tissues and therefore the release of proinflammatory mediators, thereafter leading to fibroblast activation.

Indexed as

AnimalsAntibodies, MonoclonalBiomarkersBleomycinCase-Control StudiesCells, CulturedDrug Evaluation, PreclinicalFibrosisFos-Related Antigen-2HumansHypertension, PulmonaryMice, Inbred C57BLMice, TransgenicMiddle AgedMolecular Targeted TherapyOX40 LigandAntibodies, MonoclonalBiomarkersBleomycinFosl2 protein, mouseFos-Related Antigen-2OX40 LigandTNFSF4 protein, humanTranscription Factor AP-1costimulationfibrosisOX40Lsystemic sclerosistranslational approach

Identifiers

PMID27298374
PMCPMC4941508
OpenAlexW2442421769

What OpenQuestion holds

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Registered trials

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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.