RT Journal Article
SR Electronic
T1 Disease specificity of autoantibodies to cytosolic 5′-nucleotidase 1A in sporadic inclusion body myositis versus known autoimmune diseases
JF Annals of the Rheumatic Diseases
JO Ann Rheum Dis
FD BMJ Publishing Group Ltd and European League Against Rheumatism
SP 696
OP 701
DO 10.1136/annrheumdis-2014-206691
VO 75
IS 4
A1 Megan K Herbert
A1 Judith Stammen-Vogelzangs
A1 Marcel M Verbeek
A1 Anke Rietveld
A1 Ingrid E Lundberg
A1 Hector Chinoy
A1 Janine A Lamb
A1 Robert G Cooper
A1 Mark Roberts
A1 Umesh A Badrising
A1 Jan L De Bleecker
A1 Pedro M Machado
A1 Michael G Hanna
A1 Lenka Plestilova
A1 Jiri Vencovsky
A1 Baziel G van Engelen
A1 Ger J M Pruijn
YR 2016
UL http://ard.bmj.com/content/75/4/696.abstract
AB Objectives The diagnosis of inclusion body myositis (IBM) can be challenging as it can be difficult to clinically distinguish from other forms of myositis, particularly polymyositis (PM). Recent studies have shown frequent presence of autoantibodies directed against cytosolic 5′-nucleotidase 1A (cN-1A) in patients with IBM. We therefore, examined the autoantigenicity and disease specificity of major epitopes of cN-1A in patients with sporadic IBM compared with healthy and disease controls.Methods Serum samples obtained from patients with IBM (n=238), PM and dermatomyositis (DM) (n=185), other autoimmune diseases (n=246), other neuromuscular diseases (n=93) and healthy controls (n=35) were analysed for the presence of autoantibodies using immunodominant cN-1A peptide ELISAs.Results Autoantibodies directed against major epitopes of cN-1A were frequent in patients with IBM (37%) but not in PM, DM or non-autoimmune neuromuscular diseases (<5%). Anti-cN-1A reactivity was also observed in some other autoimmune diseases, particularly Sjögren's syndrome (SjS; 36%) and systemic lupus erythematosus (SLE; 20%).Conclusions In summary, we found frequent anti-cN-1A autoantibodies in sera from patients with IBM. Heterogeneity in reactivity with the three immunodominant epitopes indicates that serological assays should not be limited to a distinct epitope region. The similar reactivities observed for SjS and SLE demonstrate the need to further investigate whether distinct IBM-specific epitopes exist.