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Research ArticleRheumatoid Arthritis

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

Kari Guderud, Marthe Thoresen Mæhlen, Gry Beate Namløs Nordang, Marte Kathrine Viken, Bettina Kulle Andreassen, Øyvind Molberg, Siri Tennebø Flåm and Benedicte Alexandra Lie
The Journal of Rheumatology September 2018, 45 (9) 1211-1219; DOI: https://doi.org/10.3899/jrheum.170769
Kari Guderud
From the Department of Medical Genetics, and the Department of Immunology, University of Oslo and Oslo University Hospital; K.G. Jebsen Inflammation Research Centre, University of Oslo; Department of Rheumatology, Oslo University Hospital; Department of Rheumatology, Diakonhjemmet Hospital; Department of Research, Cancer Registry of Norway, Institute for Population-based Research, Oslo, Norway.
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Marthe Thoresen Mæhlen
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Gry Beate Namløs Nordang
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Marte Kathrine Viken
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Bettina Kulle Andreassen
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Øyvind Molberg
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Siri Tennebø Flåm
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Benedicte Alexandra Lie
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  • For correspondence: b.a.lie@medisin.uio.no
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Abstract

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.

Key Indexing Terms:
  • RHEUMATOID ARTHRITIS
  • AUTOANTIBODIES
  • PADI4
  • ANTI-PAD4
  • ANTICITRULLINATED PROTEIN ANTIBODIES
  • Accepted for publication February 6, 2018.
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The Journal of Rheumatology: 45 (9)
The Journal of Rheumatology
Vol. 45, Issue 9
1 Sep 2018
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Lack of Association among Peptidyl Arginine Deiminase Type 4 Autoantibodies, PADI4 Polymorphisms, and Clinical Characteristics in Rheumatoid Arthritis
Kari Guderud, Marthe Thoresen Mæhlen, Gry Beate Namløs Nordang, Marte Kathrine Viken, Bettina Kulle Andreassen, Øyvind Molberg, Siri Tennebø Flåm, Benedicte Alexandra Lie
The Journal of Rheumatology Sep 2018, 45 (9) 1211-1219; DOI: 10.3899/jrheum.170769

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Lack of Association among Peptidyl Arginine Deiminase Type 4 Autoantibodies, PADI4 Polymorphisms, and Clinical Characteristics in Rheumatoid Arthritis
Kari Guderud, Marthe Thoresen Mæhlen, Gry Beate Namløs Nordang, Marte Kathrine Viken, Bettina Kulle Andreassen, Øyvind Molberg, Siri Tennebø Flåm, Benedicte Alexandra Lie
The Journal of Rheumatology Sep 2018, 45 (9) 1211-1219; DOI: 10.3899/jrheum.170769
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Keywords

RHEUMATOID ARTHRITIS
AUTOANTIBODIES
PADI4
ANTI-PAD4
ANTICITRULLINATED PROTEIN ANTIBODIES

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Keywords

  • RHEUMATOID ARTHRITIS
  • AUTOANTIBODIES
  • PADI4
  • ANTI-PAD4
  • ANTICITRULLINATED PROTEIN ANTIBODIES

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