“…Radanova et al recently demonstrated that anti-C1q antibodies from LN patients may inhibit the interaction of C1q with immobilized CRP and IgG [56]. As regards classical complement activation by surface-bound CRP, we have previously shown that this can be prevented by sufficiently high levels of fluid-phase CRP, which consumes C1q [34].…”
and nucleosomes were analyzed in pre-post flare sera. We could demonstrate that CRP, C1q, C3c and dsDNA were co-localized with IgG in electron dense deposits in the glomerular basement membrane/subendothelial space in all of the 5 LN patients.
“…Radanova et al recently demonstrated that anti-C1q antibodies from LN patients may inhibit the interaction of C1q with immobilized CRP and IgG [56]. As regards classical complement activation by surface-bound CRP, we have previously shown that this can be prevented by sufficiently high levels of fluid-phase CRP, which consumes C1q [34].…”
and nucleosomes were analyzed in pre-post flare sera. We could demonstrate that CRP, C1q, C3c and dsDNA were co-localized with IgG in electron dense deposits in the glomerular basement membrane/subendothelial space in all of the 5 LN patients.
“…The need of using high salt conditions was overcome by using the collagen-like part of C1q rather than the intact C1q molecule (Antes et al, 1988;Wener et al, 1989) or more recently linear peptides from this region (Vanhecke et al, 2012). Using dedicated experiments, anti-C1q antibodies that only target the globular head regions of C1q were more recently also described (Tsacheva et al, 2007) with possibly important functional consequences (Radanova et al, 2012).…”
“…The disease progression is associated with the presence of autoantibodies that recognize various self-molecules, including dsDNA, nuclear proteins, ribosomal proteins, and complement component C1q (1)(2)(3). These autoantibodies may appear as a result of an immune response induced by an inefficient clearance of apoptotic cells and cellular debris, which serve as a source of autoantigens.…”
Background: Autoantibodies against complement C3 are found in patients with the autoimmune disease systemic lupus erythematosus. Results: C3 autoantibodies are found in 30% of lupus nephritis patients and inhibit C3 interaction with the regulatory proteins Factor H and CR1. Conclusion: C3 autoantibodies have overt capability to overactivate complement. Significance: C3 autoantibodies can contribute to the pathological process in lupus nephritis.
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