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Matsushita, M. & Fujita, T. Cleavage of the third component of omplement (C3) by mannose-binding protein-associated serine protease (MASP) with subsequent complement activation.
Two Fabs, Fab-B4 and Fab-19, showed marked ability to inhibit the binding of BP autoantibodies and subsequent complement activation in vitro.
It appears that subsequent complement activation following anti-PEG IgM binding is the most important step in dictating the in vivo fate of PEGylated products.
With similar antigen binding activity, Fab and single-chain variable fragments (scFv) of pathogenic anti-COL17 antibodies can interfere with COL17 binding of autoantibodies, blocking subsequent complement activation and granulocyte activation.
Previous evidence supports a role for iron deficiency in the pathogenesis of gout; when iron is added to media containing urate crystals there is a stimulated oxidative stress with subsequent complement and neutrophil activation.
SpA can prevent phagocytosis by binding the complement binding portion (Fcγ) of functional antibodies thus hindering the antibody binding to bacterial cell surface components and subsequent complement dependent uptake of bacteria by phagocytic cells.
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Deficient complement-mediated IC handling increases the risk of extra-hepatic IC deposition and subsequent complement-mediated inflammation of the affected tissues [ 45].
These lesions are initiated by the binding of pathogenic aquaporin 4 (AQP4 -specific AQP4 -specific to autoantibodies subsequentocomplement-mediastrocytes of these cells.
Joint specificity is explained by the deposition of the GPI onto the articular cartilage surface, binding of anti-GPI antibodies to the surface and subsequent complement-mediated inflammation [ 22].
15 Consistent with these observations our data suggest that AQP4-IgG in CSF can achieve widespread distribution within the brain via this paravascular pathway to exert pathologic effects by selective binding to astrocytes with subsequent complement-dependent cytotoxicity that includes parenchymal BBB disruption.
The pathogenesis of GPA has not been fully elucidated, although the interaction between ANCA and neutrophils seems pivotal in initiating and supporting an inflammatory reaction with subsequent cytokine, complement, and endothelium involvement [ 3].
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