Jens Christian Jensenius

The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review


  • Anne Troldborg
  • Steffen Thiel
  • Marten Trendelenburg, University of Basel, Basel, Switzerland, Switzerland
  • Justa Friebus-Kardash, University Hospital, Basel, Switzerland, Switzerland
  • Josephine Nehring, University Hospital, Basel, Switzerland, Switzerland
  • Rudi Steffensen, Klinisk Immunologisk Afdeling, Aalborg Universitetshospital, Aarhus Universitet, Aalborg
  • ,
  • Søren Werner Karlskov Hansen, University of Southern Denmark
  • ,
  • Magdalena Janina Laska
  • Bent Deleuran
  • Jens Christian Jensenius
  • Anne Voss, Reumatologisk Afdeling, Odense Universitetshospital, Denmark
  • Kristian Stengaard-Pedersen

OBJECTIVE: The pathogenesis of systemic lupus erythematosus (SLE) involves complement activation. Activation of complement through the classical pathway (CP) is well established. However, complement activation through pattern recognition not only happens through the CP, but also through the lectin pathway (LP). We investigated the hypothesis that the LP is activated in SLE and involved in the pathogenesis of the disease.

METHODS: Using immunoassays developed in-house, we measured concentrations of LP proteins in a cohort of 372 patients with SLE and 170 controls. We estimated complement activation measuring total C3, and investigated whether LP protein concentrations were associated with complement activation and disease activity. Protein changes and disease activity over time were assessed in a cohort of 52 patients with SLE followed with repeated samples over a 5-year period.

RESULTS: Concentrations of LP proteins in SLE were altered compared with controls. The differences observed in LP proteins associated with complement activation were reflected by a decrease in total C3. The pattern recognition molecules (M-ficolin, CL-L1, and CL-K1), the serine protease (MASP-3), and the associated protein (MAp19) displayed a negative correlation with disease activity. Changes in MASP-2 concentrations over time correlated significantly with increased disease activity. Association between active proteinuria and serum concentration was observed for MASP-3 and MAp19.

CONCLUSION: In patients with SLE, we measured specific changes in LP proteins that are associated with complement activation and disease activity, indicating that the LP is activated in patients with SLE. These novel findings substantiate the involvement of the LP in SLE.

Original languageEnglish
JournalJournal of Rheumatology
Pages (from-to)1136-1144
Number of pages9
Publication statusPublished - 1 Aug 2018

Bibliographical note

doi: 10.3899/jrheum.171033.

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ID: 128378471