Evidence map›Paper›PMID 40424896›Full record

ArticleJournal of autoimmunity2025

Characterizing local antibody responses in the muscle of inclusion body myositis patients.

Sahana Jayaraman, Andrew Wilson, Xuwen Alice Zheng, Janelle M Montagne, Iago Pinal-Fernandez, Andrew L Mammen, Thomas E Lloyd, H Benjamin Larman

Abstract read
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In one paragraph

Article in Journal of autoimmunity, 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
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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

8 authors.

Sahana JayaramanInstitute for Cell Engineering, Division of Immunology, Department of Pathology, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Andrew WilsonDepartment of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Xuwen Alice ZhengInstitute for Cell Engineering, Division of Immunology, Department of Pathology, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Janelle M MontagneDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Iago Pinal-FernandezMuscle Disease Section, National Institute of Arthritis and Musculoskeletal and Skin Disease, National Institutes of Health, Bethesda, MD, USA.
Andrew L MammenMuscle Disease Section, National Institute of Arthritis and Musculoskeletal and Skin Disease, National Institutes of Health, Bethesda, MD, USA.
Thomas E LloydDepartment of Neurology, Baylor College of Medicine, Houston, TX, USA.
H Benjamin LarmanInstitute for Cell Engineering, Division of Immunology, Department of Pathology, Johns Hopkins School of Medicine, Baltimore, MD, USA. Electronic address: hlarman1@jhmi.edu.

Funding

Neurosarcoidosis: Clinical Phenotype, Biomarkers and ImmunopathogensisR01NS123712 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CARLOS A PARDO-VILLAMIZAR · 2022 to 2026
$3.3M
Design and Analysis of Displayed PeptidomesR01GM136724 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI LARMAN, HARRY BENJAMIN, RUCZINSKI, INGO · 2020 to 2023
$1.9M
NIGMS NIH HHS R01 GM136724NINDS NIH HHS R01 NS123712
6 · The paper itself

Abstract

objectiveSporadic inclusion body myositis (IBM) is the most common adult idiopathic inflammatory myopathy. IBM etiology has been elusive, due to both degenerative and autoimmune disease features found on muscle biopsy, and significant disease heterogeneity. Investigating the role of antibodies in the muscle of IBM patients may improve our understanding of disease pathogenesis.

methodsWe used an IBM xenograft mouse model in which muscle biopsy tissue from IBM patients (n = 98) and controls (n = 131; including 54 from other types of myopathy) were implanted into immunodeficient mice (NOD-Rag1

resultsWith the MSD assay we found human IgG, IgA, and IgM in a larger percentage of IBM xenografted mice versus controls. Using PhIP-Seq, we found anti-microbial reactivities secreted from IBM muscle are prevalent amongst a healthy control population but autoantigen reactivities in IBM are more unique at the peptide and protein level. Additionally, NT5C1A (IgG/IgA and IgM) and TIF1γ (IgG/A) autoantibodies are secreted from muscle tissues of 4/18 and 10/18 IBM xenograft donors, respectively.

conclusionOur characterization of antibody responses within the muscle of IBM patients reveals that muscle-infiltrating B cells produce both disease-associated autoantibodies and a broad spectrum of antibodies targeting non-self antigens.

Indexed as

Antibody FormationAutoantibodiesMuscle, SkeletalMyositis, Inclusion BodyAgedAnimalsAutoantigensBiopsyDisease Models, AnimalFemaleHumansImmunoglobulin AImmunoglobulin GImmunoglobulin MMaleMiceAutoantibodiesAutoantigensImmunoglobulin AImmunoglobulin GImmunoglobulin MAntibodiesAntibody-profiling technologiesMuscle-specific immune responseMyositisReactome profilingRepertoire sequencing

Identifiers

PMID40424896
PMCPMC12205477

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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.