Article Text

other Versions

PDF
A CLEC16A variant confers risk for juvenile idiopathic arthritis and anti-CCP negative rheumatoid arthritis
  1. Beate Skinningsrud (beate.skinningsrud{at}medisin.uio.no)
  1. Oslo University Hospital, Rikshospitalet, Norway
    1. Benedicte A Lie (b.a.lie{at}medisin.uio.no)
    1. Oslo University Hospital, Rikshospitalet, Norway
      1. Eystein S Husebye (eystein.husebye{at}med.uib.no)
      1. University of Bergen, Norway
        1. Tore K Kvien (t.k.kvien{at}medisin.uio.no)
        1. Diakonhjemmet Hospital, Norway
          1. Øystein Førre (o.t.forre{at}medisin.uio.no)
          1. Oslo University Hospital, Rikshospitalet, Norway
            1. Berit Flatø (berit.flato{at}rikshospitalet.no)
            1. Oslo University Hospital, Rikshospitalet, Norway
              1. Alice Stormyr (alice.stormyr{at}medisin.uio.no)
              1. Oslo University Hospital, Rikshospitalet, Norway
                1. Geir Joner (geir.joner{at}medisin.uio.no)
                1. Oslo University Hospital, Rikshospitalet, Norway
                  1. Pål R Njølstad (pal.njolstad{at}uib.no)
                  1. University of Bergen, Norway
                    1. Thore Egeland (thore.egeland{at}medisin.uio.no)
                    1. University of Oslo, Norway
                      1. Dag E Undlien (d.e.undlien{at}medisin.uio.no)
                      1. University of Oslo, Norway

                        Abstract

                        Objective: Variants in CLEC16A have conferred susceptibility to autoimmune diseases in genome-wide association studies. We aimed to investigate the locus’ involvement in juvenile idiopathic arthritis (JIA), and further explore the association with rheumatoid arthritis (RA), type 1 diabetes (T1D) and Addison’s disease (AD) in the Norwegian population.

                        Methods: Three SNPs were genotyped in patients with RA (n=809), JIA (n=509), T1D (n=1211) and AD (n=414), and in healthy controls (n=2149).

                        Results: All diseases were associated with CLEC16A, but with different SNPs. The intron 22 SNP, rs6498169, was associated with RA (p=0.006) and JIA (p=0.016), and the intron 19 SNPs, rs12708716/rs12917716, with T1D (p=1x10-5) and AD (p=2x10-4). The RA association was confined to the anti-CCP negative subgroup (p=2x10-4).

                        Conclusion: This is the first report of a CLEC16A association with JIA, and a split of the RA association according to anti-CCP status. Different causative variants underlie the rheumatic versus the organ specific diseases.

                        Statistics from Altmetric.com

                        Request permissions

                        If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.