Sarcoplasmic MxA expression
A valuable marker of dermatomyositis
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- Diagnosis of anti-melanoma differentiation-associated gene 5 antibody-positive dermatomyositis led by sarcoplasmic myxovirus resistance protein A expression on muscle pathology筋病理でミクソウイルス耐性蛋白質A発現筋線維を認めたことが診断の契機となった抗melanoma differentiation-associated gene 5抗体陽性皮膚筋炎の1例, Rinsho Shinkeigaku, 64, 7, (480-485), (2024).https://doi.org/10.5692/clinicalneurol.cn-001963
- Clinicopathological Reclassification of Idiopathic Inflammatory Myopathy to Match the Serological Results of Myositis-Specific Antibodies, Journal of Clinical Neurology, 20, 1, (67), (2024).https://doi.org/10.3988/jcn.2022.0432
- Pathogenic mechanisms of disease in idiopathic inflammatory myopathies: autoantibodies as clues, Frontiers in Immunology, 15, (2024).https://doi.org/10.3389/fimmu.2024.1439807
- Contribution of Complement, Microangiopathy and Inflammation in Idiopathic Inflammatory Myopathies, Journal of Neuromuscular Diseases, 11, 1, (5-16), (2024).https://doi.org/10.3233/JND-230168
- Anti-NXP2 Antibody-positive Juvenile Dermatomyositis with Characteristic Fascial Thickening on Muscle Ultrasound and Improvement with Immunotherapy, Internal Medicine, 63, 12, (1813-1817), (2024).https://doi.org/10.2169/internalmedicine.2720-23
- The Clinical Value of the Neutrophil-to-Lymphocyte Ratio, the C-Reactive Protein-to-Albumin Ratio, the Systemic Inflammatory Index, and the Systemic Inflammatory Response Index in Patients with the Anti-Synthetase Syndrome, Journal of Inflammation Research, Volume 17, (3617-3628), (2024).https://doi.org/10.2147/JIR.S460610
- Dermatomyositis: Practical Guidance and Unmet Needs, ImmunoTargets and Therapy, Volume 13, (151-172), (2024).https://doi.org/10.2147/ITT.S381472
- Clinical, histopathological features and malignancy frequency of patients with idiopathic inflammatory myopathy, Cukurova Medical Journal, 49, 2, (314-319), (2024).https://doi.org/10.17826/cumj.1412123
- Clinico‐sero‐pathological profiles and risk prediction model of idiopathic inflammatory myopathy (IIM) patients with different perifascicular changes , CNS Neuroscience & Therapeutics, 30, 8, (2024).https://doi.org/10.1111/cns.14882
- Myofibrillar myopathies due to a novel mutation in exon 8 of the LDB3 gene , International Journal of Rheumatic Diseases, 27, 2, (2024).https://doi.org/10.1111/1756-185X.15036
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Soon after our article published, [1] we found that the sale of the myxovirus resistance A (MxA) polyclonal antibodies used in the study (Mx1/2/3 [H-285], sc-50509, Santa Cruz Biotechnology, Dallas, TX) had been discontinued. Furthermore, we received inquiries from several physicians concerning alternate MxA antibodies. We tested the company's monoclonal antibody alternate (Mx1/2/3 [C-1], sc-166412) on frozen muscle sections at various dilutions in 2% bovine serum albumin in phosphate-buffered saline using the Ventana immunohistochemistry detection system (Ventana Medical Systems, Tucson, AZ) with or without the enhancement mode. Muscle samples tested included MxA-positive dermatomyositis (n=3, including 1 juvenile participant), MxA-negative dermatomyositis (n=3), anti-Jo-1 myopathy (n=3, MxA-negative), and immune-mediated necrotizing myopathy (n=3, comprising 1 with anti-signal recognition particle antibodies [MxA-negative], 1 with anti-3-hydroxy-3-methylglutaryl-CoA reductase antibodies [MxA-negative], and 1 without those antibodies [MxA-positive]). We observed essentially the same staining pattern at comparable signal intensity as the original polyclonal antibodies at 1:10 dilution with the enhancement mode although the signal was barely detected at the manufacturer's recommended dilution (starting dilution: 1:50), indicating that the monoclonal antibody alternate can be similarly used to detect sarcoplasmic MxA expression on frozen muscle sections for the diagnosis of dermatomyositis (albeit higher concentration is necessary).
1. Uruha A, Nishikawa A, Tsuburaya RS, et al. Sarcoplasmic MxA expression: A valuable marker of dermatomyositis. Neurology Epub 2016 Dec 30.
For disclosures, please contact the editorial office at [email protected].