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2015 ; 182
(2
): 132-8
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Collectin liver 1 and collectin kidney 1 and other complement-associated pattern
recognition molecules in systemic lupus erythematosus
#MMPMID26154564
Troldborg A
; Thiel S
; Jensen L
; Hansen S
; Laska MJ
; Deleuran B
; Jensenius JC
; Stengaard-Pedersen K
Clin Exp Immunol
2015[Nov]; 182
(2
): 132-8
PMID26154564
show ga
The objective of this study 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. 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 immunoflourometric assays. The SLE patients' demographic,
diagnostic, clinical and biochemical data and collection of plasma samples were
performed prospectively during 4 months. CL-L1, CL-K1 and M-ficolin plasma
concentrations were lower in SLE patients than healthy controls (P-values <
0.001, 0.033 and < 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). 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.
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