Evidence map›Paper›PMID 40976864›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2026

Autoantibody Response Toward Chromatin in Patients With Juvenile Idiopathic Arthritis.

Viola Pitkänen, Terhi Remes-Pakarinen, Paula Vähäsalo, Milja Möttönen, Minna-Maija Grönlund, Miika Arvonen, Mikael Knip, Riitta Veijola, Jorma Toppari, Jorma Ilonen and 4 more

Abstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 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.

Viola PitkänenUniversity of Eastern Finland, Kuopio, Finland.
Terhi Remes-PakarinenKuopio University Hospital, Kuopio.
Paula VähäsaloOulu University Hospital and University of Oulu, Oulu, Finland.
Milja MöttönenUniversity of Turku and Turku University Hospital, Turku, Finland.
Minna-Maija GrönlundUniversity of Turku and Turku University Hospital, Turku, Finland.
Miika ArvonenKuopio University Hospital, Kuopio.
Mikael KnipTampere University Hospital, Tampere, and University of Helsinki, Helsinki, Finland.
Riitta VeijolaOulu University Hospital and University of Oulu, Oulu, Finland.
Jorma ToppariUniversity of Turku and Turku University Hospital, Turku, Finland.
Jorma IlonenUniversity of Turku, Turku, Finland.
Johanna LempainenUniversity of Turku and Turku University Hospital, Turku, Finland.
Anna-Mari SchroderusUniversity of Eastern Finland, Kuopio, Finland.
Liisa KrögerKuopio University Hospital, Kuopio.
Tuure KinnunenUniversity of Eastern Finland and ISLAB Laboratory Centre, Kuopio, Finland.ORCID 0000-0003-1595-5371

Funding

ISLAB Laboratory Centre N/ALastentautien Tutkimussäätiö N/APäivikki ja Sakari Sohlbergin Säätiö N/A
6 · The paper itself

Abstract

objectivePatients with juvenile idiopathic arthritis (JIA) frequently exhibit antinuclear antibodies (ANAs), but the specific antigen target recognized by them and the presence of additional autoantibody specificities in patients with JIA remains elusive.

methodsPlasma samples from 110 untreated patients with active JIA, as well as from 14 children with unspecified arthritis and 151 age- and sex-matched healthy children, were analyzed with multiple modern clinical-grade autoantibody assays, including automated indirect immunofluorescence to screen for ANAs with HEp-2 cells, and specific immune assays to detect reactivity to individual autoantigens. In addition, a HuProt proteome microarray was used to screen for novel autoantibody targets in plasma samples from five patients with ANA-positive JIA and four ANA-negative healthy controls.

resultsHomogeneous nuclear ANA staining, indicating reactivity toward chromatin, was detected in most (61.8%) patients with JIA but rarely in healthy controls (2.6%; P < 0.0001). No antibody reactivity to specific nuclear antigens or other autoantigens associated with connective tissue diseases was detected. However, 20% of patients with JIA harbored antibodies against double-stranded DNA (dsDNA)-nucleosome complexes (compared with 2.6% of controls, P < 0.0001). Finally, the proteome microarray revealed core histone H2A variant H2AFY, part of the nucleosome, to be the most widely recognized human protein by autoantibodies of patients with JIA.

conclusionAutoantibody reactivity in JIA primarily targets chromatin, but the epitopes targeted are likely either posttranslationally modified or multimolecule epitopes, such as dsDNA-nucleosome complexes, rather than epitopes on individual native proteins or purified dsDNA.

Indexed as

Antibodies, AntinuclearArthritis, JuvenileAutoantibodiesChromatinAdolescentAutoantigensCase-Control StudiesChildChild, PreschoolFemaleFluorescent Antibody Technique, IndirectHumansMaleAntibodies, AntinuclearAutoantibodiesAutoantigensChromatin

Identifiers

PMID40976864
PMCPMC12936893

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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.