Affiliation:
1. National Institute of Arthritis and Musculoskeletal and Skin Diseases National Institutes of Health Bethesda Maryland
2. Johns Hopkins University School of Medicine Baltimore Maryland
3. NIH Clinical Center, National Institutes of Health Bethesda Maryland
4. National Institute of Arthritis and Musculoskeletal and Skin Diseases National Institutes of Health, Bethesda, and Johns Hopkins University School of Medicine Baltimore Maryland
5. National Institute of Environmental Health Sciences National Institutes of Health Bethesda Maryland
Abstract
ObjectiveNovel autoantibody specificities including anti‐CCAR1 were recently discovered in adult patients with anti‐transcriptional intermediary factor (TIF1)–positive dermatomyositis (DM) and were associated with attenuated cancer emergence. The aims of the present study were to examine whether these autoantibodies occur in patients with juvenile‐onset DM (JDM) and to determine their associated features.MethodsSera from 150 patients with anti‐TIF1γ autoantibody‐positive JDM in a cross‐sectional cohort and 90 juvenile healthy controls were assayed for anti‐CCAR1, anti‐C1Z1, anti‐IMMT, anti‐TBL1XR1, and anti‐Sp4 autoantibodies. Demographics, myositis autoantibodies, clinical features, medications, outcomes, and HLA‐DRB1 and HLA‐DQA1 alleles were compared between those with and without these autoantibodies.ResultsAny one of the anti‐TIF1γ‐associated autoantibodies was present in 44 patients (29%) overall, including 25 (17%) with anti‐Sp4, 22 (15%) with anti‐TBL1XR1, 14 (9%) with anti‐CCAR1, 2 (1%) with anti‐C1Z1, and 2 (1%) with anti‐IMMT autoantibodies. These anti‐TIF1γ‐associated autoantibodies frequently co‐occurred. Patients with any of the anti‐TIF1γ‐associated autoantibodies had less frequent falling (34% [15] vs. 53% [56], P = 0.032) and lower peak muscle enzymes. None of the patients had cancer. Among White patients, HLA‐DRB1*03 was protective against an anti‐TIF1γ‐associated autoantibody (odds ratio 0.20, 95% confidence interval 0.07–0.52).ConclusionAutoantibodies associated with anti‐TIF1γ were found in isolation and in combination among a subset of patients with JDM. Patients with these autoantibodies had less severe muscle disease and were not enriched for HLA‐DRB1*03. Additional autoantibodies among patients with positive anti‐TIF1γ with JDM likely contribute to the heterogeneity of the anti‐TIF1γ serologic subgroup.
Funder
Donald B. and Dorothy L. Stabler Foundation
National Institute of Arthritis and Musculoskeletal and Skin Diseases
National Institute of Environmental Health Sciences
Clinical Center
Subject
Immunology,Rheumatology,Immunology and Allergy
Cited by
2 articles.
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