Lack of Association among Peptidyl Arginine Deiminase Type 4 Autoantibodies, PADI4 Polymorphisms, and Clinical Characteristics in Rheumatoid Arthritis

We aimed to jointly investigate the role of antipeptidyl arginine deiminase type 4 antibodies (anti-PAD4) and polymorphisms in the gene together with clinical variables in rheumatoid arthritis (RA). Serum IgG autoantibodies to human recombinant PAD4 were identified by DELFIA technique in 745 patient...

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Bibliographic Details
Published in:Journal of rheumatology 2018-08, Vol.45 (9), p.1211-1219
Main Authors: Guderud, Kari, Mæhlen, Marthe Thoresen, Nordang, Gry Beate Namløs, Viken, Marte Kathrine, Andreassen, Bettina Kulle, Molberg, Øyvind, Flåm, Siri Tennebø, Lie, Benedicte Alexandra
Format: Article
Language:English
Subjects:
Adult
Aged
Arthritis, Rheumatoid - blood
Arthritis, Rheumatoid - genetics
Arthritis, Rheumatoid - immunology
Autoantibodies
Epitopes
Female
Genetic Predisposition to Disease
Genotype
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide
Protein-Arginine Deiminase Type 4
Protein-Arginine Deiminases - genetics
Protein-Arginine Deiminases - immunology
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Summary:We aimed to jointly investigate the role of antipeptidyl arginine deiminase type 4 antibodies (anti-PAD4) and polymorphisms in the gene together with clinical variables in rheumatoid arthritis (RA). Serum IgG autoantibodies to human recombinant PAD4 were identified by DELFIA technique in 745 patients with RA (366 available from previous studies). Genotyping of was performed using TaqMan assays in 945 patients and 1118 controls. Clinical data, anticitrullinated protein antibodies (ACPA) status, shared epitope status, and a combined genetic risk score were also available. Anti-PAD4 antibodies were detected in 193 (26%) of 745 patients with RA; 149 (77%) of these were also ACPA-positive. No association was observed between anti-PAD4 status and clinical characteristics, polymorphisms, or genetic risk scores after stratification for ACPA status. Taken together, the results from these combined serological, genetic, and clinical analyses suggest that anti-PAD4 appears to be a bystander autoantibody with no current clinical utility in RA.
ISSN:0315-162X
1499-2752
DOI:10.3899/jrheum.170769