Evidence map›Paper›PMID 42550610›Full record

ArticleJCI insight2026

IFN-γ-producing self-reactive CD4+ T cells induce autoimmune adrenalitis in a mouse model of Addison's disease.

Arina Andreyeva, Juraj Michalik, Veronika Niederlova, Veronika Cimermanova, Ales Drobek, Radislav Sedlacek, Jan Prochazka, Juraj Labaj, Olha Fedosieieva, Waldemar Kanczkowski and 4 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in JCI insight, 2026. 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

14 authors.

Arina AndreyevaLaboratory of Adaptive Immunity, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czechia.
Juraj MichalikLaboratory of Adaptive Immunity, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czechia.
Veronika NiederlovaLaboratory of Adaptive Immunity, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czechia.
Veronika CimermanovaLaboratory of Adaptive Immunity, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czechia.
Ales DrobekLaboratory of Adaptive Immunity, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czechia.
Radislav SedlacekCzech Centre for Phenogenomics & Laboratory of Transgenic Models of Diseases, Institute of Molecular Genetics of the Czech Academy of Sciences, Vestec, Czechia.
Jan ProchazkaCzech Centre for Phenogenomics & Laboratory of Transgenic Models of Diseases, Institute of Molecular Genetics of the Czech Academy of Sciences, Vestec, Czechia.
Juraj LabajCzech Centre for Phenogenomics & Laboratory of Transgenic Models of Diseases, Institute of Molecular Genetics of the Czech Academy of Sciences, Vestec, Czechia.
Olha FedosieievaCzech Centre for Phenogenomics & Laboratory of Transgenic Models of Diseases, Institute of Molecular Genetics of the Czech Academy of Sciences, Vestec, Czechia.
Waldemar KanczkowskiDepartment of Internal Medicine III, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Peter DraberDepartment of Immunobiology, University of Lausanne, Epalinges, Switzerland.
André SulenDepartment of Clinical Science, Faculty of Medicine, University of Bergen, Norway.
Ondrej StepanekLaboratory of Adaptive Immunity, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czechia.
Aleš NeuwirthLaboratory of Adaptive Immunity, Institute of Molecular Genetics of the Czech Academy of Sciences, Prague, Czechia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune Addison's disease (AD) is a rare but life-threatening disorder caused by immune-mediated destruction of the adrenal cortex, and progress in therapy has been limited by insufficient mechanistic insight. Here, we establish a model of experimental autoimmune adrenalitis that recapitulates key features of AD and reveals sex-dependent differences in disease manifestation within the model. Immunization with peptides derived from the adrenal self-antigen CYP11A1 induces corticosterone insufficiency. We show that autoimmune adrenalitis is driven by IFN-γ produced by self-reactive CD4+ T cells, promoting granulomatous inflammation in the adrenal cortex. Together, these findings identify IFN-γ as a central effector of autoimmune adrenalitis and suggest that targeting the IFN-γ pathway may represent a potential therapeutic strategy for AD.

Indexed as

Addison DiseaseAutoimmune DiseasesCD4-Positive T-LymphocytesInterferon-gammaAdrenal CortexAnimalsAutoantigensDisease Models, AnimalFemaleMaleMiceAutoantigensInterferon-gammaAutoimmune diseasesAutoimmunityClinical ResearchEndocrinologyMolecular pathology

Identifiers

PMID42550610
PMCPMC13596732

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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.