ACR Meeting Abstracts

ACR Meeting Abstracts

  • Meetings
    • ACR Convergence 2024
    • ACR Convergence 2023
    • 2023 ACR/ARP PRSYM
    • ACR Convergence 2022
    • ACR Convergence 2021
    • ACR Convergence 2020
    • 2020 ACR/ARP PRSYM
    • 2019 ACR/ARP Annual Meeting
    • 2018-2009 Meetings
    • Download Abstracts
  • Keyword Index
  • Advanced Search
  • Your Favorites
    • Favorites
    • Login
    • View and print all favorites
    • Clear all your favorites
  • ACR Meetings

Abstract Number: 522

Genetic Variation in the NCR3 Locus Is Associated with Anti-SSA⁄SSB Positive Primary Sjögren′s Syndrome in Scandinavian Samples

Gunnel Nordmark1, Maija-Leena Eloranta1, Per Eriksson2, Elke Theander3, Helena Forsblad-d'Elia4, Roald Omdal5, Marie Wahren-Herlenius6, Roland Jonsson7 and Lars Rönnblom1, 1Rheumatology, Department of Medical Sciences, Uppsala University, Uppsala, Sweden, 2Rheumatology/AIR, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden, 3Dept of Rheumatology, Skane University Hospital, Lund University, Malmö, Sweden, 4Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden, 5Department of Internal Medicine, Stavanger university Hospital, Stavanger, Clinical Immunology Unit, Department of Internal Medicine, Stavanger University Hospital, Stavanger, Norway, 6Dept of Medicine, Karolinska Institutet, Stockholm, Sweden, 7Broegelmann Research Laboratory, the Gade Institute, University of Bergen, Bergen, Norway

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: genomics, human leukocyte antigens (HLA), natural killer (NK) cells and polymorphism, Sjogren's syndrome

  • Tweet
  • Click to email a link to a friend (Opens in new window) Email
  • Click to print (Opens in new window) Print
Session Information

Title: Sjögren's Syndrome - Pathogenesis

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Candidate gene studies in primary Sjögren’s syndrome (pSS) have identified polymorphisms in genes involved in the type I interferon (IFN) system and the type I IFN system is activated in pSS. NK cells have been shown to increase the immune complex stimulated IFN-alpha production by plasmacytoid dendritic cells but the role for NK cells in pSS autoimmunity has not been well studied. The natural cytotoxicity triggering receptor 3 (NCR3) gene locus (6p21.3) encodes the NKp30 activating receptor on NK cells. A French study identified an association between two rare alleles in the NCR3 promoter region and pSS, independent of the association to HLA-DRB1-03 (6p21.3) (1). The aim of this investigation was to analyze if the two NCR3 single nucleotide polymorphisms (SNPs) were associated with pSS in Scandinavian samples. The potential association with anti-SSA/SSB positivity or clinical phenotypes was investigated. In addition, the association with the HLA-DRB1-03 SNP proxy was studied.

Methods:

A total of 671 Caucasian pSS patients from Sweden (n=478) and Norway (n=193) and 1586 healthy controls (Sweden, n=1369 and Norway, n=217) were included in the study. Two SNPs in the NCR3 locus, rs11575837 and rs2736191 and the SNP rs2187668 as a marker for HLA-DRB1-03 were selected. Genotyping was performed by single base extension with Fluorescent Polarization Template Dye Incorporation (FP-TDI). Data on anti-SSA and/or anti-SSB positivity and clinical manifestations were extracted from the patient files. Case-control and case-only allelic association analyses were performed using PLINK.

Results:

In our case-control analysis we did not find any association between the NCR3 SNPs and pSS in Sweden or Norway or in meta-analysis of the two cohorts. In case-only analysis of the combined cohorts, comparing anti-SSA/SSB positive (n=496, 74%) versus negative (n=175, 26%) pSS patients, we found an association between the SNP rs11575837 and anti-SSA/SSB positivity, p=0.006, OR 0.27 (95% CI 0.10-0.73). There were no associations between the NCR3 SNPs and clinical phenotype. The HLA-DRB1-03 SNP marker rs2187668 was strongly associated with pSS, p=1×10-51, OR 3.2 (95% CI 2.8-3.8). When analyzing only anti-SSA/SSB positive patients versus controls the association was even stronger, p=6.9×10-67, OR 4.1 (95% CI 3.5-4.9). In case-only analysis rs2187668 was associated with major salivary gland swelling and leucopenia (p<0.05), dermal vasculitis (p<0.01), hypergammaglobulinemia (p=7.4x10-8) and anti-SSA/SSB positivity (p=1.6×10-12, OR 3.0, 95% CI 2.2-4.1).

Conclusion:

We found an association between anti-SSA/SSB positivity and genetic variation in the NCR3 locus and confirmed the strong HLA-DRB1-03 association with anti-SSA/SSB positive pSS. We conclude that different mechanisms, possibly involving NK cell functions, might contribute to this autoimmune disease in anti-SSA/SSB positive versus negative patients. The potential functional implications for this rare promoter SNP on NKp30 receptor activity has yet to be elucidated.

References:

1. Miceli-Richard et al. Ann Rheum Dis 2011;70(Suppl3):212


Disclosure:

G. Nordmark,
None;

M. L. Eloranta,
None;

P. Eriksson,
None;

E. Theander,
None;

H. Forsblad-d’Elia,
None;

R. Omdal,
None;

M. Wahren-Herlenius,
None;

R. Jonsson,
None;

L. Rönnblom,
None.

  • Tweet
  • Click to email a link to a friend (Opens in new window) Email
  • Click to print (Opens in new window) Print

« Back to 2012 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/genetic-variation-in-the-ncr3-locus-is-associated-with-anti-ssa%e2%81%84ssb-positive-primary-sjogren%e2%80%b2s-syndrome-in-scandinavian-samples/

Advanced Search

Your Favorites

You can save and print a list of your favorite abstracts during your browser session by clicking the “Favorite” button at the bottom of any abstract. View your favorites »

All abstracts accepted to ACR Convergence are under media embargo once the ACR has notified presenters of their abstract’s acceptance. They may be presented at other meetings or published as manuscripts after this time but should not be discussed in non-scholarly venues or outlets. The following embargo policies are strictly enforced by the ACR.

Accepted abstracts are made available to the public online in advance of the meeting and are published in a special online supplement of our scientific journal, Arthritis & Rheumatology. Information contained in those abstracts may not be released until the abstracts appear online. In an exception to the media embargo, academic institutions, private organizations, and companies with products whose value may be influenced by information contained in an abstract may issue a press release to coincide with the availability of an ACR abstract on the ACR website. However, the ACR continues to require that information that goes beyond that contained in the abstract (e.g., discussion of the abstract done as part of editorial news coverage) is under media embargo until 10:00 AM ET on November 14, 2024. Journalists with access to embargoed information cannot release articles or editorial news coverage before this time. Editorial news coverage is considered original articles/videos developed by employed journalists to report facts, commentary, and subject matter expert quotes in a narrative form using a variety of sources (e.g., research, announcements, press releases, events, etc.).

Violation of this policy may result in the abstract being withdrawn from the meeting and other measures deemed appropriate. Authors are responsible for notifying colleagues, institutions, communications firms, and all other stakeholders related to the development or promotion of the abstract about this policy. If you have questions about the ACR abstract embargo policy, please contact ACR abstracts staff at [email protected].

Wiley

  • Online Journal
  • Privacy Policy
  • Permissions Policies
  • Cookie Preferences

© Copyright 2025 American College of Rheumatology