ArticleThe American journal of pathology2011
Inclusion body myositis: laser microdissection reveals differential up-regulation of IFN-γ signaling cascade in attacked versus nonattacked myofibers.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 51 citations in OpenAlex.
- Trial
- Emerging therapies in idiopathic inflammatory myopathies.Journal of neuromuscular diseases · 2026Review
- Soluble SIGLEC1 as a biomarker of disease activity in idiopathic inflammatory myopathies.Rheumatology (Oxford, England) · 2026Article
- Energy metabolism dysregulation in idiopathic inflammatory myopathies: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Inclusion body myositis, viral infections, and TDP-43: a narrative review.Clinical and experimental medicine · 2024Review
- Influence of Inflammatory Cytokines IL-1Mediators of inflammation · 2023Article
- Impaired muscle strength is associated with ultrastructure damage in myositis.Scientific reports · 2022Article
- Inclusion Body Myositis and Neoplasia: A Narrative Review.International journal of molecular sciences · 2022Review
- Muscle Transcriptomics Shows Overexpression of Cadherin 1 in Inclusion Body Myositis.Annals of neurology · 2022Article
- Identification of Regulatory Factors and Prognostic Markers in Amyotrophic Lateral Sclerosis.Antioxidants (Basel, Switzerland) · 2022Article
- The role of interferons type I, II and III in myositis: A review.Brain pathology (Zurich, Switzerland) · 2021Review
- Inflammatory myopathies: update on diagnosis, pathogenesis and therapies, and COVID-19-related implications.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2020Review
- Machine learning algorithms reveal unique gene expression profiles in muscle biopsies from patients with different types of myositis.Annals of the rheumatic diseases · 2020Article
- Identification of distinctive interferon gene signatures in different types of myositis.Neurology · 2019Article
- Inclusion body myositis: clinical features and pathogenesis.Nature reviews. Rheumatology · 2019Review
- Review
- Proteomic Profiling Unravels a Key Role of Specific Macrophage Subtypes in Sporadic Inclusion Body Myositis.Frontiers in immunology · 2019Article
- Article
- Transcriptional profiling identifies differential expression of long non-coding RNAs in Jo-1 associated and inclusion body myositis.Scientific reports · 2017Article
- Immune and myodegenerative pathomechanisms in inclusion body myositis.Annals of clinical and translational neurology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sporadic inclusion body myositis (IBM) is a muscle disease with two separate pathogenic components, degeneration and inflammation. Typically, nonnecrotic myofibers are focally surrounded and invaded by CD8(+) T cells and macrophages. Both attacked and nonattacked myofibers express high levels of human leukocyte antigen class I (HLA-I) molecules, a prerequisite for antigen presentation to CD8(+) T cells. However, only a subgroup of HLA-I(+) myofibers is attacked by immune cells. By using IHC, we classified myofibers from five patients with sporadic IBM as attacked (A(IBM)) or nonattacked (N(IBM)) and isolated the intracellular contents of myofibers separately by laser microdissection. For comparison, we isolated myofibers from control persons (H(CTRL)). The samples were analyzed by microarray hybridization and quantitative PCR. HLA-I up-regulation was observed in A(IBM) and N(IBM), whereas H(CTRL) were negative for HLA-I. In contrast, the inducible chain of the interferon (IFN) γ receptor (IFNGR2) and several IFN-γ-induced genes were up-regulated in A(IBM) compared with N(IBM) and H(CTRL) fibers. Confocal microscopy confirmed segmental IFNGR2 up-regulation on the membranes of A(IBM), which positively correlated with the number of adjacent CD8(+) T cells. Thus, the differential up-regulation of the IFN-γ signaling cascade observed in the attacked fibers is related to local inflammation, whereas the ubiquitous HLA-I expression on IBM muscle fibers does not require IFNGR expression.
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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.