Evidence map›Paper›PMID 41194220›Full record

ArticleArthritis research & therapy2025

Dual impact of interleukin-17 A blockade on inflammatory and stromal pathways in peripheral spondyloarthritis.

Ihsan Hammoura, Renée H Fiechter, Leonieke J J van Mens, Henriëtte M Y de Jong, Inka A Fluri, Sander W Tas, Dominique L P Baeten, Marleen G H van de Sande, Nataliya G Yeremenko

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Article in Arthritis research & therapy, 2025. 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. Article
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

9 authors.

Ihsan HammouraDepartment of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, Location AMC, University of Amsterdam, Amsterdam, The Netherlands.
Renée H FiechterDepartment of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, Location AMC, University of Amsterdam, Amsterdam, The Netherlands.
Leonieke J J van MensDepartment of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, Location AMC, University of Amsterdam, Amsterdam, The Netherlands.
Henriëtte M Y de JongDepartment of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, Location AMC, University of Amsterdam, Amsterdam, The Netherlands.
Inka A FluriDepartment of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, Location AMC, University of Amsterdam, Amsterdam, The Netherlands.
Sander W TasDepartment of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, Location AMC, University of Amsterdam, Amsterdam, The Netherlands.
Dominique L P BaetenDepartment of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, Location AMC, University of Amsterdam, Amsterdam, The Netherlands.
Marleen G H van de Sande *Department of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, Location AMC, University of Amsterdam, Amsterdam, The Netherlands. m.g.vandesande@amsterdamumc.nl.
Nataliya G Yeremenko *Department of Rheumatology and Clinical Immunology, Amsterdam Rheumatology and Immunology Center, Amsterdam University Medical Centers, Location AMC, University of Amsterdam, Amsterdam, The Netherlands.

Funding

Marie Skłodowska-Curie grant agreement 847551NWO ZonMW VENI 09150161810112
6 · The paper itself

Abstract

backgroundIL-17 A plays a role in the pathology of spondyloarthritis (SpA), as evidenced by the clinical efficacy of IL-17 A inhibitors (IL-17Ai). Nevertheless, the exact role of IL-17 A in driving synovial inflammation and pathological remodeling remains unknown. In this study, we investigated the molecular pathways affected by IL-17Ai in SpA synovitis to determine whether this response is tissue- and/or treatment-specific.

methodsSynovial biopsies from 12 peripheral SpA (pSpA) patients before and after 12 weeks of IL-17Ai treatment were analyzed by RNA-sequencing and qPCRs. The synovial tissue response to IL-17Ai in 7 psoriatic arthritis (PsA) patients was compared to open-source gene expression data of skin biopsies from 15 psoriasis (PsO) patients treated with IL-17Ai, and synovial biopsies from 7 PsA patients receiving IL-12p40/IL-23p40 blockade.

resultsCompared to baseline, IL-17Ai significantly modulated the expression of 1255 genes (549 upregulated and 706 downregulated, FDR < 0.1) in the synovium at week 12. The downregulated genes were predominantly associated with inflammatory processes and stromal functions. Comprehensive analysis revealed that IL-17Ai-mediated suppression of bone remodeling is independent of its inhibition of inflammatory pathways. While IL-17Ai consistently attenuated inflammation-related pathways in both psoriatic joints and skin, its effect on bone remodeling pathways was specific to the synovium. This distinguishes IL-17Ai from IL-12p40/IL-23p40 inhibitors, which, while mitigating synovial inflammation, did not affect tissue remodeling.

conclusionsOur findings provide new insights into the molecular mechanisms of IL-17 A blockade in pSpA, underscoring its unique role in selectively targeting bone-remodeling processes specific to the joints of individuals with SpA.

Indexed as

Interleukin-17SpondylarthritisAdultArthritis, PsoriaticFemaleHumansInflammationMaleMiddle AgedSignal TransductionSynovial MembraneIL17A protein, humanInterleukin-17IL-17A inhibitorsPeripheral spondyloarthritisPsoriatic skinStromal pathwaysSynovium

Identifiers

PMID41194220
PMCPMC12587550

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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.