OBJECTIVE: To compare the binding of immune complexes and anti-Clq in systemic lupus erythematosus (SLE) sera to Clq and to the purified collagen-like region of Clq (CLR) in high and physiologic NaCl concentrations. METHODS: Sera from patients with SLE were tested for binding of IgG to Clq and to CLR in physiologic (0.15 M NaCl) or high (1.0 M NaCl) salt concentration. Sera were ultracentrifuged to separate monomeric IgG and high molecular weight IgG (immune complexes), and fractions were tested for binding to C1q and to CLR in the presence of physiologic or high salt concentrations. RESULTS: Decrease in binding of immune complexes to Clq in the presence of high salt ranged from 0 to 96.8%, with a median of 48.4%. Decrease of the binding of monomeric IgG to C1q in the presence of high salt ranged from 2.2 to 74.3%, with a median of 46.2%. Binding of monomeric autoantibodies to CLR also was decreased by high salt. Nevertheless, anti-Clq measured by binding to CLR in physiologic salt correlated highly with the binding to Clq in both physiologic (r = 0.978) and high salt (r = 0.983). CONCLUSION: Clq-binding of immune complexes in SLE sera is not uniformly abrogated by high salt and binding of autoantibodies to CLR is variably reduced by high salt. Binding of IgG to Clq in high salt correlates with but is not equivalent to quantifying these autoantibodies by binding to CLR.
OBJECTIVE: To compare the binding of immune complexes and anti-Clq in systemic lupus erythematosus (SLE) sera to Clq and to the purified collagen-like region of Clq (CLR) in high and physiologic NaCl concentrations. METHODS: Sera from patients with SLE were tested for binding of IgG to Clq and to CLR in physiologic (0.15 M NaCl) or high (1.0 M NaCl) salt concentration. Sera were ultracentrifuged to separate monomeric IgG and high molecular weight IgG (immune complexes), and fractions were tested for binding to C1q and to CLR in the presence of physiologic or high salt concentrations. RESULTS: Decrease in binding of immune complexes to Clq in the presence of high salt ranged from 0 to 96.8%, with a median of 48.4%. Decrease of the binding of monomeric IgG to C1q in the presence of high salt ranged from 2.2 to 74.3%, with a median of 46.2%. Binding of monomeric autoantibodies to CLR also was decreased by high salt. Nevertheless, anti-Clq measured by binding to CLR in physiologic salt correlated highly with the binding to Clq in both physiologic (r = 0.978) and high salt (r = 0.983). CONCLUSION:Clq-binding of immune complexes in SLE sera is not uniformly abrogated by high salt and binding of autoantibodies to CLR is variably reduced by high salt. Binding of IgG to Clq in high salt correlates with but is not equivalent to quantifying these autoantibodies by binding to CLR.
Authors: D Saadoun; S Sadallah; M Trendelenburg; N Limal; D Sene; J C Piette; J A Schifferli; P Cacoub Journal: Clin Exp Immunol Date: 2006-08 Impact factor: 4.330
Authors: L A Trouw; M A Seelen; R Visseren; J M G J Duijs; H Benediktsson; E de Heer; A Roos; C van Kooten; M R Daha Journal: Clin Exp Immunol Date: 2004-01 Impact factor: 4.330
Authors: Leendert A Trouw; Tom W L Groeneveld; Marc A Seelen; Jacques M G J Duijs; Ingeborg M Bajema; Frans A Prins; Uday Kishore; David J Salant; J Sjef Verbeek; Cees van Kooten; Mohamed R Daha Journal: J Clin Invest Date: 2004-09 Impact factor: 14.808
Authors: Daniel J Birmingham; Joshua E Bitter; Ezinne G Ndukwe; Sarah Dials; Terese R Gullo; Sara Conroy; Haikady N Nagaraja; Brad H Rovin; Lee A Hebert Journal: Clin J Am Soc Nephrol Date: 2015-12-23 Impact factor: 8.237