PT  - JOURNAL ARTICLE
AU  - Kari Guderud
AU  - Marthe Thoresen  Mæhlen
AU  - Gry Beate Namløs  Nordang
AU  - Marte Kathrine  Viken
AU  - Bettina Kulle  Andreassen
AU  - Øyvind Molberg
AU  - Siri Tennebø  Flåm
AU  - Benedicte Alexandra  Lie
TI  - Lack of Association among Peptidyl Arginine Deiminase Type 4 Autoantibodies, <em>PADI4</em> Polymorphisms, and Clinical Characteristics in Rheumatoid Arthritis
AID  - 10.3899/jrheum.170769
DP  - 2018 Jun 01
TA  - The Journal of Rheumatology
PG  - jrheum.170769
4099  - http://www.jrheum.org/content/early/2018/05/25/jrheum.170769.short
4100  - http://www.jrheum.org/content/early/2018/05/25/jrheum.170769.full
AB  - Objective We aimed to jointly investigate the role of antipeptidyl arginine deiminase type 4 antibodies (anti-PAD4) and polymorphisms in the PADI4 gene together with clinical variables in rheumatoid arthritis (RA). Methods Serum IgG autoantibodies to human recombinant PAD4 were identified by DELFIA technique in 745 patients with RA (366 available from previous studies). Genotyping of PADI4 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. Results 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, PADI4 polymorphisms, or genetic risk scores after stratification for ACPA status. Conclusion 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.