ArticleActa neuropathologica communications2013
Comparative utility of LC3, p62 and TDP-43 immunohistochemistry in differentiation of inclusion body myositis from polymyositis and related inflammatory myopathies.
Article in Acta neuropathologica communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.
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51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- Emerging therapies in idiopathic inflammatory myopathies.Journal of neuromuscular diseases · 2026Review
- Energy metabolism dysregulation in idiopathic inflammatory myopathies: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- [Not just frailty-Sjögren's syndrome and polymyositis with mitochondrial pathology].Zeitschrift fur Rheumatologie · 2025Article
- Alpha-Synuclein as a Potential Biomarker for Inclusion Body Myositis in Blood and Muscle.Neuropathology and applied neurobiology · 2025Article
- Loss of TDP-43 Splicing Repression Occurs in Myonuclei of Inclusion Body Myositis Patients.Annals of neurology · 2025Article
- Inclusion body myositis and immunosenescence: current evidence and future perspectives.Rheumatology (Oxford, England) · 2025Review
- The clinical features, muscle pathology, and role of autophagy in anti-Ku-positive patients.Frontiers in immunology · 2025Article
- Seeding-competent TDP-43 persists in human patient and mouse muscle.Science translational medicine · 2024Article
- Current biomarkers in inclusion body myositis.Journal of neuromuscular diseases · 2024Review
- Seeding competent TDP-43 persists in human patient and mouse muscle.bioRxiv : the preprint server for biology · 2024Article
- Sporadic Inclusion Body Myositis at the Crossroads between Muscle Degeneration, Inflammation, and Aging.International journal of molecular sciences · 2024Review
- Amplifying the Heat Shock Response Ameliorates ALS and FTD Pathology in Mouse and Human Models.Molecular neurobiology · 2023Article
- Cytotoxic immune cells do not affect TDP-43 and p62 sarcoplasmic aggregation but influence TDP-43 localisation.Scientific reports · 2023Article
- Article
- Unravelling inclusion body myositis using a patient-derived fibroblast model.Journal of cachexia, sarcopenia and muscle · 2023Article
- Neuromuscular disease: 2023 update.Free neuropathology · 2023Article
- COVID-19-Associated Critical Illness Myopathy with Direct Viral Effects.Annals of neurology · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInclusion body myositis (IBM) is a slowly progressive inflammatory myopathy of the elderly that does not show significant clinical improvement in response to steroid therapy. Distinguishing IBM from polymyositis (PM) is clinically important since PM is steroid-responsive; however, the two conditions can show substantial histologic overlap.
resultsWe performed quantitative immunohistochemistry for (1) autophagic markers LC3 and p62 and (2) protein aggregation marker TDP-43 in 53 subjects with pathologically diagnosed PM, IBM, and two intermediate T cell-mediated inflammatory myopathies (polymyositis with COX-negative fibers and possible IBM). The percentage of stained fibers was significantly higher in IBM than PM for all three immunostains, but the markers varied in sensitivity and specificity. In particular, both LC3 and p62 were sensitive markers of IBM, but the tradeoff between sensitivity and specificity was smaller (and diagnostic utility thus greater) for LC3 than for p62. In contrast, TDP-43 immunopositivity was highly specific for IBM, but the sensitivity of this test was low, with definitive staining present in just 67% of IBM cases.
conclusionsTo differentiate IBM from PM, we thus recommend using a panel of LC3 and TDP-43 antibodies: the finding of <14% LC3-positive fibers helps exclude IBM, while >7% of TDP-43-positive fibers strongly supports a diagnosis of IBM. These data provide support for the hypothesis that disruption of autophagy and protein aggregation contribute to IBM pathogenesis.
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