ArticlePloS one2012
Autoantibodies produced at the site of tissue damage provide evidence of humoral autoimmunity in inclusion body myositis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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.
Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Emerging therapies in idiopathic inflammatory myopathies.Journal of neuromuscular diseases · 2026Review
- Identification of distinct immune signatures in inclusion body myositis by peripheral blood immunophenotyping using machine learning models.Clinical & translational immunology · 2024Article
- The Plasma Cell Infiltrate Populating the Muscle Tissue of Patients with Inclusion Body Myositis Features Distinct B Cell Receptor Repertoire Properties.ImmunoHorizons · 2023Article
- Skeletal muscle fibers produce B-cell stimulatory factors in chronic myositis.Frontiers in immunology · 2023Article
- The Role of Immune Cells in the Pathogenesis of Idiopathic Inflammatory Myopathies.Aging and disease · 2021Review
- Affinity maturation is required for pathogenic monovalent IgG4 autoantibody development in myasthenia gravis.The Journal of experimental medicine · 2020Article
- Autoantibodies targeting TRIM72 compromise membrane repair and contribute to inflammatory myopathy.The Journal of clinical investigation · 2020Article
- Inclusion body myositis: clinical features and pathogenesis.Nature reviews. Rheumatology · 2019Review
- Anti-NT5c1A Autoantibodies as Biomarkers in Inclusion Body Myositis.Frontiers in immunology · 2019Article
- Autoantibody-producing plasmablasts after B cell depletion identified in muscle-specific kinase myasthenia gravis.JCI insight · 2017Article
- Development of autoantibodies against muscle-specific FHL1 in severe inflammatory myopathies.The Journal of clinical investigation · 2015Article
- Amyloid deposits and inflammatory infiltrates in sporadic inclusion body myositis: the inflammatory egg comes before the degenerative chicken.Acta neuropathologica · 2015Review
- Investigating the Antigen Specificity of Multiple Sclerosis Central Nervous System-Derived Immunoglobulins.Frontiers in immunology · 2015Article
- Diagnosis, pathogenesis and treatment of myositis: recent advances.Clinical and experimental immunology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 8 institutions in 2 countries.
Funding
Abstract
Inclusion body myositis (IBM) belongs to a group of muscle diseases known as the inflammatory myopathies. The presence of antibody-secreting plasma cells in IBM muscle implicates the humoral immune response in this disease. However, whether the humoral immune response actively contributes to IBM pathology has not been established. We sought to investigate whether the humoral immune response in IBM both in the periphery and at the site of tissue damage was directed towards self-antigens. Peripheral autoantibodies present in IBM serum but not control serum recognized self-antigens in both muscle tissue and human-derived cell lines. To study the humoral immune response at the site of tissue damage in IBM patients, we isolated single plasma cells directly from IBM-derived muscle tissue sections and from these cells, reconstructed a series of recombinant immunoglobulins (rIgG). These rIgG, each representing a single muscle-associated plasma cell, were examined for reactivity to self-antigens. Both, flow cytometry and immunoblotting revealed that these rIgG recognized antigens expressed by cell lines and in muscle tissue homogenates. Using a mass spectrometry-based approach, Desmin, a major intermediate filament protein, expressed abundantly in muscle tissue, was identified as the target of one IBM muscle-derived rIgG. Collectively, these data support the view that IBM includes a humoral immune response in both the periphery and at the site of tissue damage that is directed towards self-antigens.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.