Evidence map›Paper›PMID 39595046›Full record

ArticleBiomedicines2024

Dexamethasone's Clinical Efficacy in Experimental Autoimmune Pancreatitis Correlates with a Unique Transcriptomic Signature, Whilst Kinase Inhibitors Are Not Effective.

Ottavia Agrifoglio, Anika Kasprick, Natalie Gross, Marc Wahlig, Emilia Kauffold, Aline Woitas, Artem Vorobyev, Luise Ehlers, Ralf J Ludwig, Katja Bieber and 1 more

Abstract read
In one paragraph

Article in Biomedicines, 2024. 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. Frontiers in immunology · 2025
    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

11 authors.

Ottavia AgrifoglioDepartment of Medicine II, Division of Gastroenterology and Endocrinology, Rostock University Medical Center, 18057 Rostock, Germany.
Anika KasprickLübeck Institute of Experimental Dermatology and Center for Research on Inflammation of the Skin, University of Lübeck, 23562 Lübeck, Germany.
Natalie GrossLübeck Institute of Experimental Dermatology and Center for Research on Inflammation of the Skin, University of Lübeck, 23562 Lübeck, Germany.ORCID 0000-0003-0773-3285
Marc WahligDepartment of Medicine II, Division of Gastroenterology and Endocrinology, Rostock University Medical Center, 18057 Rostock, Germany.
Emilia KauffoldDepartment of Medicine II, Division of Gastroenterology and Endocrinology, Rostock University Medical Center, 18057 Rostock, Germany.
Aline WoitasDepartment of Medicine II, Division of Gastroenterology and Endocrinology, Rostock University Medical Center, 18057 Rostock, Germany.
Artem VorobyevDepartment of Dermatology, University of Lübeck, 23562 Lübeck, Germany.ORCID 0000-0002-1542-0732
Luise EhlersDepartment of Medicine II, Division of Gastroenterology and Endocrinology, Rostock University Medical Center, 18057 Rostock, Germany.
Ralf J LudwigLübeck Institute of Experimental Dermatology and Center for Research on Inflammation of the Skin, University of Lübeck, 23562 Lübeck, Germany.
Katja BieberLübeck Institute of Experimental Dermatology and Center for Research on Inflammation of the Skin, University of Lübeck, 23562 Lübeck, Germany.ORCID 0000-0002-3855-6683
Robert JasterDepartment of Medicine II, Division of Gastroenterology and Endocrinology, Rostock University Medical Center, 18057 Rostock, Germany.ORCID 0000-0002-8220-4570

Funding

Deutsche Forschungsgemeinschaft 253137138; EXC 2167State of Schleswig Holstein Schleswig-Holstein Excellence-Chair Program
6 · The paper itself

Abstract

(1) Background: Autoimmune pancreatitis (AIP) is mainly treated with steroids. Using an AIP mouse model, we investigated two potential alternatives, the transforming growth factor-β-activated kinase 1 inhibitor, takinib, and the Janus kinase inhibitor, tofacitinib. (2) Methods: In a multicenter preclinical study, MRL/MpJ mice were injected with polyinosinic/polycytidylic acid (poly I:C) for two weeks to induce AIP. They were then treated for four weeks with either takinib (25, 50, or 75 mg/kg body weight), tofacitinib (5, 10 or 15 mg/kg), dexamethasone (1 mg/kg), or solvent, while the poly I:C injections were continued. The severity of AIP was assessed histopathologically. Flow cytometry was used to examine lymphocyte subtypes in the spleen and mesenteric lymph nodes. The pancreatic gene expression profiles were analyzed by RNA sequencing. (3) Results: Poly I:C-treated mice developed severe AIP with inflammation, destruction of acinar tissue, and fibrosis. Dexamethasone significantly attenuated the disease, while takinib or tofacitinib had no effects. Dexamethasone also antagonized the effects of poly I:C on the relative frequencies of the AIP-associated lymphocyte subtypes CD4/CD69, CD8/CD44

Indexed as

autoimmune pancreatitisdexamethasoneMRL/Mp mousetakinibtofacitinibtranscriptome

Identifiers

PMID39595046
PMCPMC11591683

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.