Evidence map›Paper›PMID 40405219›Full record

ArticleImmunity & ageing : I & A2025

Diverging effects of tumor necrosis factor inhibitors and conventional synthetic disease-modifying antirheumatic drugs on immunosenescence and inflammageing in rheumatoid arthritis: a cross-sectional analysis.

Tobias Schwarz, Giovanni Almanzar, Sebastian Völkl, Martin Feuchtenberger, Johannes Leierer, Christian Schmidt, Frank Deininger, Hans-Peter Tony, Marc Schmalzing, Martina Prelog

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity & ageing : I & A, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. 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

10 authors.

Tobias SchwarzDepartment of Pediatrics, Pediatric Rheumatology and Special Immunology, University Hospital Würzburg, University of Würzburg, Würzburg, Germany.
Giovanni AlmanzarDepartment of Pediatrics, Pediatric Rheumatology and Special Immunology, University Hospital Würzburg, University of Würzburg, Würzburg, Germany.
Sebastian VölklDepartment of Pediatrics, Pediatric Rheumatology and Special Immunology, University Hospital Würzburg, University of Würzburg, Würzburg, Germany.
Martin FeuchtenbergerDepartment of Internal Medicine II, Rheumatology/Clinical Immunology, University Hospital Würzburg, University of Würzburg, Würzburg, Germany.
Johannes LeiererDepartment of Internal Medicine IV (Nephrology and Hypertension), Medical University Innsbruck, Innsbruck, Austria.
Christian SchmidtDepartment of Haematology and Oncology, University of Greifswald, Greifswald, Germany.
Frank DeiningerPractice for Rheumatology, Haugerpfarrgasse 7, Würzburg, Germany.
Hans-Peter TonyDepartment of Internal Medicine II, Rheumatology/Clinical Immunology, University Hospital Würzburg, University of Würzburg, Würzburg, Germany.
Marc SchmalzingDepartment of Internal Medicine II, Rheumatology/Clinical Immunology, University Hospital Würzburg, University of Würzburg, Würzburg, Germany.
Martina PrelogDepartment of Pediatrics, Pediatric Rheumatology and Special Immunology, University Hospital Würzburg, University of Würzburg, Würzburg, Germany. martina.prelog@uni-wuerzburg.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmunosenescence is characterized by a decline in naive T cells, a reduced T cell receptor repertoire, and the accumulation of terminally-differentiated and unspecifically-activated proinflammatory cells, a process called inflammageing. Premature immunosenescence is thought to be pathogenetically relevant in rheumatoid arthritis (RA), either by posing a risk factor for its development, or by advancing the rheumatic disease as a result of excess antigenic and inflammatory stimulation. We investigated parameters of immunosenescence in RA patients treated with conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) only compared to patients treated additionally or exclusively with a tumor necrosis factor inhibitor (TNFi) and age-matched healthy controls to investigate the effect of RA treatment on age-associated T cell phenotypes and functions.

resultsThe csDMARD-only treated patients, compared to the TNFi-treated patients and healthy controls, displayed an enhanced age-dependent decline in CD31

conclusionsWhereas a TNFi treatment seems to counteract the non-inflammatory aspects of immunosenescence, it induces increasing proportions of terminally-differentiated, cytokine-producing effector memory T cells, requiring awareness as possibly contributing to secondary autoimmune phenomena in RA.

Indexed as

Conventional synthetic disease-modifying antirheumatic drugImmunosenescenceInflammageingRheumatoid arthritisTumor necrosis factor inhibitor

Identifiers

PMID40405219
PMCPMC12096643

What Socratic 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 Socratic graph.