ArticleArthritis & rheumatology (Hoboken, N.J.)2017
Immune-Array Analysis in Sporadic Inclusion Body Myositis Reveals HLA-DRB1 Amino Acid Heterogeneity Across the Myositis Spectrum.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 3 of them syntheses that pooled it.
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Who cites it
33 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Efficacy and safety of pharmacological treatments in inclusion body myositis: a systematic review.RMD open · 2025Pooled it
- Genetics of idiopathic inflammatory myopathies: insights into disease pathogenesis.Current opinion in rheumatology · 2019Pooled it
- Association of HLA-DR, HLA-DQ, and HLA-B alleles with inclusion body myositis risk: A systematic review, a meta-analysis, a meta-regression and a trial sequential analysis.International journal of immunopathology and pharmacologyPooled it
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- Distinct cytokine and cytokine receptor expression patterns characterize different forms of myositis.Rheumatology (Oxford, England) · 2025Article
- HLA loci heterozygosity modulates genetic risk in idiopathic inflammatory myopathies.Annals of the rheumatic diseases · 2025Article
- Genetics of myositis - distinct backgrounds of subtypes.Journal of human genetics · 2025Review
- Inflammatory Myopathies and Autoimmune Gluten-related Disorders: A Scoping Review of Pathophysiological Interconnections and Hypothesis.Recent advances in inflammation & allergy drug discovery · 2025Article
- Occupational and Hobby Exposures Associated With Myositis Phenotypes in a National Myositis Patient Registry.Arthritis care & research · 2025Article
- Discovery of new myositis genetic associations through leveraging other immune-mediated diseases.HGG advances · 2024Article
- Inclusion body myositis, viral infections, and TDP-43: a narrative review.Clinical and experimental medicine · 2024Review
- Pathologic Features of Anti-Ku Myositis.Neurology · 2024Article
- Epidemiology of the idiopathic inflammatory myopathies.Nature reviews. Rheumatology · 2023Review
- Identification of Novel Associations and Localization of Signals in Idiopathic Inflammatory Myopathies Using Genome-Wide Imputation.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- Inclusion body myositis: from genetics to clinical trials.Journal of neurology · 2023Review
- Muscle Transcriptomics Shows Overexpression of Cadherin 1 in Inclusion Body Myositis.Annals of neurology · 2022Article
- Loss of TDP-43 function and rimmed vacuoles persist after T cell depletion in a xenograft model of sporadic inclusion body myositis.Science translational medicine · 2022Article
- Identification of Hub Genes and Biological Pathways in Inclusion Body Myositis Using Bioinformatics Analysis.International journal of general medicine · 2022Article
- The Genetics of Autoimmune Myositis.Frontiers in immunology · 2022Review
- Inclusion body myositis: Update on the diagnostic and therapeutic landscape.Frontiers in neurology · 2022Review
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Authors and funding
33 authors.
Funding
Abstract
objectiveInclusion body myositis (IBM) is characterized by a combination of inflammatory and degenerative changes affecting muscle. While the primary cause of IBM is unknown, genetic factors may influence disease susceptibility. To determine genetic factors contributing to the etiology of IBM, we conducted the largest genetic association study of the disease to date, investigating immune-related genes using the Immunochip.
methodsA total of 252 Caucasian patients with IBM were recruited from 11 countries through the Myositis Genetics Consortium and compared with 1,008 ethnically matched controls. Classic HLA alleles and amino acids were imputed using SNP2HLA.
resultsThe HLA region was confirmed as the most strongly associated region in IBM (P = 3.58 × 10
conclusionThis is the largest, most comprehensive genetic association study to date in IBM. The data confirm that HLA is the most strongly associated region and identifies novel amino acid associations that may explain the risk in this locus. These amino acid associations differentiate IBM from polymyositis and dermatomyositis and may determine properties of the peptide-binding groove, allowing it to preferentially bind autoantigenic peptides. A novel suggestive association within the chromosome 3 p21.31 region suggests a role for CCR5.
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