Evidence map›Paper›PMID 40778135›Full record

ArticlemedRxiv : the preprint server for health sciences2025

Anti-TRIM72 Autoantibodies in Idiopathic Inflammatory Myopathies.

Eugene Krustev, Tiara N Safaei, Daniela Trejo-Zambrano, Lisa Christopher-Stine, Andrew Mammen, Julie J Paik, Jemima Albayda, Christopher A Mecoli, Brittany L Adler, Noah Weisleder and 3 more

Abstract readPreprint
In one paragraph

Article in medRxiv : the preprint server for health sciences, 2025. 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

13 authors.

Eugene KrustevJohns Hopkins University School of Medicine, Baltimore, MD.
Tiara N SafaeiJohns Hopkins Department of Chemical and Biomolecular Engineering, Baltimore, MD.
Daniela Trejo-ZambranoJohns Hopkins University School of Medicine, Baltimore, MD.
Lisa Christopher-StineJohns Hopkins University School of Medicine, Baltimore, MD.
Andrew MammenJohns Hopkins University School of Medicine, Baltimore, MD.
Julie J PaikJohns Hopkins University School of Medicine, Baltimore, MD.
Jemima AlbaydaJohns Hopkins University School of Medicine, Baltimore, MD.
Christopher A MecoliJohns Hopkins University School of Medicine, Baltimore, MD.
Brittany L AdlerJohns Hopkins University School of Medicine, Baltimore, MD.
Noah WeislederUniversity of Kentucky College of Medicine, Department of Molecular & Cellular Biology, Lexington, KY.
Wael JarjourThe Ohio State University College of Medicine, Department of Internal Medicine, Columbus, OH.
Brendan AntiochosJohns Hopkins University School of Medicine, Baltimore, MD.
Eleni TiniakouJohns Hopkins University School of Medicine, Baltimore, MD.

Funding

Phenotype-Specific Immune Responses in the Systemic VasculitidesP30AR053503 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI BINGHAM, CLIFTON O · 2006 to 2015
$6.4M
The Retroelement LINE1 and the DNA Sensor IF16 in Sjogren's SyndromeK08AR077100 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI ANTIOCHOS, BRENDAN · 2021 to 2025
$794k
RNA: Polymerase III specific CD8+ T cells: a mechanistic insight into cancer-induced autoimmunity in sclerodermaK08AR077732 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TINIAKOU, ELENI · 2021 to 2025
$794k
NIAMS NIH HHS K08 AR077100NIAMS NIH HHS K08 AR077732NIAMS NIH HHS P30 AR053503
6 · The paper itself

Abstract

Background and Purpose-: Tripartite motif-containing protein 72 (TRIM72) mediates tissue-repair following injury in several organs, including muscle and lung. Autoantibodies directed against TRIM72 (anti-TRIM72) have been identified in patients with idiopathic inflammatory myopathies (IIM) and disrupt TRIM72 function Methods-: Sera from IIM patient (antisynthetase syndrome [ASyS], immune mediated necrotizing myopathy [IMNM], and dermatomyositis [DM]) and healthy controls (HC) were included. Anti-TRIM72 autoantibodies were tested using enzyme linked immunosorbent assay. Anti-TRIM72 testing was positive if value was >2 standard deviations above the mean for HC. Clinicodemographic features were identified through chart review and compared between anti-TRIM72 positive (anti-TRIM72[+]) and negative (anti-TRIM72[-]) groups. Results-: Anti-TRIM72 levels were significantly increased in patients with ASyS and IMNM when compared to patients with DM and healthy controls. Anti-TRIM72 levels were also increased in patients expressing anti-Jo-1, anti-PL7, anti-HMGCR, anti-SRP, and anti-MDA5. In ASyS, when anti-TRIM72(+) and anti-TRIM72(-) patients were compared, there were significantly more anti-TRIM72(+) ASyS patients with normal DLCO (>75%) when compared to anti-TRIM72(-); however, there were no differences in demographic features, CK levels or FVC. In anti-HMGCR(+) IMNM, anti-TRIM72(+) was associated with a lower proportion of females, as well as older age at time of diagnosis and at time of anti-TRIM72 testing; however, there was no significant difference in other clinicodemographic features in anti-HMGCR(+) IMNM patients when anti-TRIM72(+) and anti-TRIM72(-) groups were compared. Conclusions-: Anti-TRIM72 antibody titres are increased in patients with ASyS and IMNM. The presence of anti-TRIM72 antibodies was not associated with a more severe phenotype in ASyS or anti-HMGCR(+) IMNM, and there were more ASyS patients with normal DLCO in the anti-TRIM72(+) group.

Identifiers

PMID40778135
PMCPMC12330466

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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.