Evidence map›Paper›PMID 42091395›Full record

ArticleAnnals of the rheumatic diseases2026

Myeloid dendritic cell subsets characterise muscle in patients with inclusion body myositis and correlate with the IFN-γ pathway and effector T cell markers.

Raphael A Kirou, Iago Pinal-Fernandez, Maria Casal-Dominguez, Katherine Pak, Chiseko Ikenaga, Christopher Nelke, Sven Wischnewski, Corinna Preusse, Stefania Del Orso, Faiza Naz and 9 more

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Article in Annals of the rheumatic diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors.

Raphael A KirouMuscle Disease Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA; College of Medicine, State University of New York Downstate Health Sciences University, Brooklyn, New York, USA.
Iago Pinal-FernandezMuscle Disease Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Maria Casal-DominguezMuscle Disease Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Katherine PakMuscle Disease Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Chiseko IkenagaDepartment of Cell Biology and Anatomy, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Christopher NelkeDepartment of Neurology, University Hospital Düsseldorf, Düsseldorf, Germany; Division of Neuroimmunology, Department of Neurology, BG University Hospital Bergmannsheil, Ruhr University Bochum, Bochum, Germany; Heimer Institute for Muscle Research, BG University Hospital Bergmannsheil, Bochum, Germany.
Sven WischnewskiDepartment of Neurology, Heidelberg University, Mannheim, Germany.
Corinna PreusseDepartment of Neuropathology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Stefania Del OrsoGenomic Technology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Faiza NazDepartment of Neuropathology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Shamima IslamGenomic Technology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Gustavo Gutierrez-CruzGenomic Technology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Thomas E LloydDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Lucas SchirmerDepartment of Neurology, Heidelberg University, Mannheim, Germany; Mannheim Center for Translational Neuroscience and Institute for Innate Immunoscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Tobias RuckDepartment of Neurology, University Hospital Düsseldorf, Düsseldorf, Germany; Division of Neuroimmunology, Department of Neurology, BG University Hospital Bergmannsheil, Ruhr University Bochum, Bochum, Germany; Heimer Institute for Muscle Research, BG University Hospital Bergmannsheil, Bochum, Germany.
Werner StenzelDepartment of Neurology, Charité-Universitätsmedizin Berlin, Corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH), Berlin, Germany.
Albert Selva-O'CallaghanSystemic Autoimmune Disease Unit, Vall d'Hebron Institute of Research, Barcelona, Spain; Internal Medicine Department, Autonomous University of Barcelona, Barcelona, Spain.
Jose C MilisendaInternal Medicine Department, Muscle Research Unit, Hospital Clinic, Barcelona, Spain; Department of Medicine, Barcelona University, Barcelona, Spain; Center for Biomedical Network Research on Rare Diseases (CIBERER), Barcelona, Spain.
Andrew L MammenMuscle Disease Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Electronic address: andrew.mammen@nih.gov.

Funding

Muscle Disease UnitZIAAR041203 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI MAMMEN, ANDREW · 2015 to 2025
$19.7M
Intramural NIH HHS ZIA AR041203
6 · The paper itself

Abstract

objectivesInclusion body myositis (IBM) is an idiopathic inflammatory myopathy characterised by type 1 inflammation, driven by muscle-infiltrating KLRG1+ and TBX21+ cytotoxic T cells. However, the cellular sources of the stimuli that trigger this effector response in the muscle of patients with IBM remain unclear. Given their role as antigen-presenting cells, we hypothesised that these may be myeloid dendritic cells (mDCs), which have previously been reported in skeletal muscle of patients with IBM. We used immunohistochemistry, immunofluorescence, single-nucleus RNA-sequencing (snRNA-seq) and bulk RNA-sequencing (RNA-seq) data from skeletal muscle of patients with IBM, other myositis, and controls to identify mDCs and characterise their contribution to IBM inflammation.

methodsWe first analysed snRNA-seq data from 3 datasets to identify, quantify, and characterise 3 mDC subsets: type 1 conventional dendritic (cDC1) cells, type 2 conventional dendritic (cDC2) cells, and mature immunoregulatory dendritic (mregDC) cells. We then analysed RNA-seq data from 2 datasets to correlate specific markers of these subsets with markers of IBM disease activity. We used immunohistochemistry and immunofluorescence to confirm mDC presence.

resultsAll 3 mDC subsets, and especially cDC1 cells, are relatively increased in the muscle of patients with IBM and correlate strongly with IBM-specific inflammatory markers, including KLRG1 and TBX21. In particular, cDC1 cells specifically express the KLRG1 ligands, CDH1 and CDH2, and, along with mregDC cells, IL12B, representing possible juxtacrine and paracrine signals for effector T cells in IBM.

conclusionsSkeletal muscle of patients with IBM is specifically characterised by mDC subsets that correlate with markers of cytotoxic T cells and type 1 inflammation.

Indexed as

Dendritic CellsInterferon-gammaMuscle, SkeletalMyositis, Inclusion BodyBiomarkersFemaleHumansMaleSignal TransductionT-Box Domain ProteinsBiomarkersInterferon-gammaT-Box Domain Proteins

Identifiers

PMID42091395
PMCPMC13251529

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