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Front Immunol. 2018 Jun 5;9:1200. doi: 10.3389/fimmu.2018.01200. eCollection 2018.

Autoantibodies to Cytosolic 5'-Nucleotidase 1A in Primary Sjögren's Syndrome and Systemic Lupus Erythematosus.

Author information

1
Department of Neurology, Center for Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, Netherlands.
2
Laboratory of Translational Immunology, Department of Rheumatology and Clinical Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
3
Laboratorio di Patologia Clinica, Ospedale San Antonio, Azienda Sanitaria Universitaria Integrata di Udine, Tolmezzo, Italy.
4
Institute for Experimental Immunology, Euroimmun AG, Lübeck, Germany.
5
Service de physiologie et d'explorations fonctionnelles, Service de rhumatologie, Centre de référence des maladies auto-immunes rares and Fédération de médecine translationnelle de Strasbourg, Université de Strasbourg, Strasbourg, France.
6
Department of Autoimmunology and Biomarkers, Statens Serum Institut, Copenhagen, Denmark.
7
Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden and Department of Rheumatology, Skåne University Hospital, Malmö, Sweden.
8
Copenhagen Lupus and Vasculitis Clinic, Centre for Rheumatology and Spine Disease, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
9
Department of Biomolecular Chemistry, Radboud Institute for Molecular Life Sciences and Institute for Molecules and Materials, Radboud University, Nijmegen, Netherlands.

Abstract

Introduction:

Autoantibodies to cytosolic 5'-nucleotidase 1A (cN-1A; NT5C1A) have a high specificity when differentiating sporadic inclusion body myositis from polymyositis and dermatomyositis. In primary Sjögren's syndrome (pSS) and systemic lupus erythematosus (SLE) anti-cN-1A autoantibodies can be detected as well. However, various frequencies of anti-cN-1A reactivity have been reported in SLE and pSS, which may at least in part be explained by the different assays used. Here, we determined the occurrence of anti-cN-1A reactivity in a large number of patients with pSS and SLE using one standardized ELISA.

Methods:

Sera from pSS (n = 193) and SLE patients (n = 252) were collected in five European centers. Anti-cN-1A, anti-Ro52, anti-nucleosome, and anti-dsDNA reactivities were tested by ELISA (Euroimmun AG) in a single laboratory. Correlations of anti-cN-1A reactivity with demographic data and clinical data (duration of disease at the moment of serum sampling, autoimmune comorbidity and presence of muscular symptoms) were analyzed using SPSS software.

Results:

Anti-cN-1A autoantibodies were found on average in 12% of pSS patients, with varying frequencies among the different cohorts (range: 7-19%). In SLE patients, the anti-cN-1A positivity on average was 10% (range: 6-21%). No relationship was found between anti-cN-1A reactivity and the presence or absence of anti-Ro52, anti-nucleosome, and anti-dsDNA reactivity in both pSS and SLE. No relationship between anti-cN-1A reactivity and duration of disease at the moment of serum sampling and the duration of serum storage was observed. The frequency of muscular symptoms or viral infections did not differ between anti-cN-1A-positive and -negative patients. In both disease groups anti-cN-1A-positive patients suffered more often from other autoimmune diseases than the anti-cN-1A-negative patients (15 versus 5% (p = 0.05) in pSS and 50 versus 30% (p = 0.02) in SLE).

Conclusion:

Our results confirm the relatively frequent occurrence of anti-cN-1A in pSS and SLE patients and the variation in anti-cN-1A reactivity between independent groups of these patients. The explanation for this variation remains elusive. The correlation between anti-cN-1A reactivity and polyautoimmunity should be evaluated in future studies. We conclude that anti-cN-1A should be classified as a myositis-associated-, not as a myositis-specific-autoantibody based on its frequent presence in SLE and pSS.

KEYWORDS:

Cytosolic 5′-nucleotidase 1A; NT5C1A; Sjögren’s syndrome; anti-cN-1A; autoantibodies; inclusion body myositis; systemic lupus erythematosus

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