Jens Christian Jensenius

CL-L1 and CL-K1 and other complement associated pattern recognition molecules in systemic lupus erythematosus

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OBJECTIVE: The objective was to explore the involvement of collectin liver 1 (CL-L1) and collectin kidney 1 (CL-K1) and other pattern recognition molecules (PRMs) of the lectin pathway of the complement system in a cross-sectional cohort of Systemic Lupus Erythematosus (SLE) patients.

METHODS: Concentrations in plasma of CL-L1, CL-K1, mannan-binding lectin (MBL), M-ficolin, H-ficolin and L-ficolin were determined in 58 patients with SLE and 65 healthy controls using time resolved immuno-flourometric assays. The SLE patients' demographic, diagnostic, clinical, and biochemical data, and collection of plasma samples were done prospectively during 4 months.

RESULTS: CL-L1, CL-K1 and M-ficolin plasma concentrations were lower in SLE patients than healthy controls (p values <0.001, 0.033 and p<0.001, respectively). H-ficolin concentration was higher in SLE patients (p<0.0001). CL-L1 and CL-K1 plasma concentrations in the individuals correlated in both patients and controls. Patients with low complement component 3 (C3) demonstrated a negative correlation between C3 and CL-L1 and CL-K1 (p=0.022 and 0.031 respectively). Patients positive for anti-dsDNA-antibodies had lower levels of MBL in plasma than patients negative for anti-dsDNA-antibodies (p=0.02).

CONCLUSION: In a cross-sectional cohort of SLE patients, we found differences in the plasma concentrations of CL-L1, CL-K1, M-ficolin and H-ficolin compared to a group of healthy controls. Alterations in plasma concentrations of the PRMs of the lectin pathway in SLE patients and associations to key elements of the disease support the hypothesis that the lectin pathway plays a role in the pathogenesis of SLE. This article is protected by copyright. All rights reserved.

TidsskriftClinical and Experimental Immunology
StatusUdgivet - 7 jul. 2015

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