Evidence map›Paper›PMID 42445175›Full record

ArticleFrontiers in immunology2026

PDE4 inhibitor mitigates activated CD8+ T cells through NF-κB signaling in Behçet's syndrome.

Alexandre Le Joncour, Paul Régnier, Anna Maciejewski-Duval, Erwan Charles, Cloé Comarmond, Stéphane Barete, Matheus Vieira, Pierre Fouret, Alexandre Belot, Sébastien Viel and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 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

14 authors.

Alexandre Le JoncourSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.
Paul RégnierSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.
Anna Maciejewski-DuvalSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.
Erwan CharlesSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.
Cloé ComarmondSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.
Stéphane BareteSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.
Matheus VieiraSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.
Pierre FouretCenter of Research on Inflammation, CNRS ERL 8252, Université de Paris, Sorbonne Paris Cite, Laboratoire d'excellence INFLAMEX, Paris, France.
Alexandre BelotPaediatric Rheumatology, Nephrology, Dermatology Unit, National Reference Centre for Rheumatism and Systemic Autoimmune Diseases in Children RAISE, Hospices Civils de Lyon, Lyon, France.
Sébastien VielImmunology Laboratory, National Reference Centre for Rheumatism and Systemic Autoimmune Diseases in Children RAISE, Hospices Civils de Lyon, Pierre Bénite, France.
Michelle RosenzwajgSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.
David KlatzmannSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.
Patrice CacoubSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.
David SaadounSorbonne Université, INSERM, UMR S 959, Immunology-Immunopathology- Immunotherapy (I3); Laboratoire d'excellence TRANSIMMUNOM, RHU iMAP, Paris, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: Behçet's disease (BD) is a systemic vasculitis with inflammatory lesions mediated by cytotoxic T cells and neutrophils. Here, we explore the critical involvement of NF-κB signaling pathway in proinflammatory CD8+ T cells differentiation and disease progress of BD patients. Methods: We performed microarray gene expression analyses, flow cytometry, immunophenotyping, immunohistochemistry and functional assessments of CD8+ T cells from BD patients and HD. Results: Transcriptionally, among the 6,595 up-regulated genes in CD8+ T cells of BD vs HD, we highlighted a great enrichment for pathways linked to NF-κB and TLR signaling (i.e. Conclusion: We highlighted that activated CD8+ T cells through NF-κB signaling pathway are instrumental in BD.

Indexed as

Behcet SyndromeCD8-Positive T-LymphocytesLymphocyte ActivationNF-kappa BPhosphodiesterase 4 InhibitorsSignal TransductionAdultFemaleHumansMaleMiddle AgedNF-kappa BPhosphodiesterase 4 Inhibitorsapremilastbehçet diseaseCD8NFkappaBPDE4 inhibition

Identifiers

PMID42445175
PMCPMC13359495

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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.