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Sjögren syndrome
Original article
SIGLEC1 is a biomarker of disease activity and indicates extraglandular manifestation in primary Sjögren's syndrome
  1. Thomas Rose1,
  2. Franziska Szelinski1,
  3. Anna Lisney1,
  4. Karin Reiter1,
  5. Sarah J Fleischer1,
  6. Gerd R Burmester1,
  7. Andreas Radbruch2,
  8. Falk Hiepe1,
  9. Andreas Grützkau2,
  10. Robert Biesen1 and
  11. Thomas Dörner1
  1. 1Department of Rheumatology and Clinical Immunology, Charité Universitätsmedizin Berlin, Berlin, Germany
  2. 2German Rheumatism Research Center (DRFZ) Berlin, a Leibniz Institute, Berlin, Germany
  1. Correspondence to Professor Thomas Dörner, Department of Rheumatology and Clinical Immunology, Charité Universitätsmedizin Berlin, Charitéplatz 1—Berlin 10117, Germany; Thomas.Doerner{at}charite.de

Abstract

Objectives To evaluate the interferon (IFN) biomarkers sialic acid binding Ig like lectin 1 (SIGLEC1, CD169) and IFN-γ-inducible protein-10 (IP-10) in patients with primary Sjögren's syndrome (pSS).

Methods 31 patients fulfilling the American-European criteria for pSS were included. Disease activity was obtained by EULAR Sjögren's syndrome disease activity index (ESSDAI). SIGLEC1 expression on monocytes was analysed using flow cytometry. IP-10 concentrations were determined using Bioplex human Cytokine 27-plex kit. Spearman rank test (SRT) was used for correlation analysis and Mann-Whitney U (MWU) to test for differences between glandular and extraglandular manifestations.

Results An activated IFN system was detected by an upregulation of SIGLEC1 expression in 64.5% and by elevated serum level of IP-10 in 78.9% of our patients with pSS. In a subsequent analysis SIGLEC1 expression was found to be upregulated more frequently in patients with extraglandular manifestations (16/16, 100%) compared to patients with exclusively glandular involvement (4/15, 27%). SIGLEC1 expression could significantly discriminate between these two disease subgroups (p=0.0001, MWU) with a positive predictive value (PPV) of 80% for extraglandular disease. Moreover, the expression correlated with disease activity (p=0.005, r=0.54, SRT). Serum IP-10 levels neither differed significantly between glandular and extraglandular disease nor correlated with ESSDAI.

Conclusions Our results indicate that increased SIGLEC1 expression characterises patients with systemic involvement and high disease activity. Therefore, SIGLEC1 determination might be of value for subset definition, risk stratification and differential therapeutic considerations in pSS.

  • Sjøgren's Syndrome
  • Inflammation
  • Disease Activity
  • Cytokines

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

https://doi.org/10.1136/rmdopen-2016-000292

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    Footnotes

    • TR and FS contributed equally.

    • Contributors TD proposed the study, contributed to the design of the study, clinical assessment, recruitment of patients; interpretation of the findings and drafting of the manuscript. TR contributed to clinical assessment and recruitment of patients, carried out the statistical analysis, the interpretation of the findings and preparation and drafting of the manuscript. FS performed the experimental analysis, contributed to the interpretation of the findings, to the manuscript preparation/drafting and interpretation of the findings. AL, KR and SJF contributed to the acquisition of data and contributed to the interpretation of the findings and to the manuscript preparation. GB, AR, FH, RB and AG contributed to interpretation of findings and critical review of the mansucript. All authors provided substantial contributions to the design or the acquisition, analysis, or interpretation of data of the study. All authors participated in revising the mansucript critically and approved the version to be published.

    • Funding Deutsche Forschungsgemeinschaft -DFG -SF650, IMMUNOBONE Do491/8-2, Do491/7-2,3.

    • Competing interests None declared.

    • Ethics approval Ethics committee of the Charité Berlin approved the study.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Data sharing statement No additional data are available.