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Formation of the MAC is controlled by complement regulatory molecules, such as CD59, vitronectin and clusterin.
Concentrations of the complement systems' components (CS) determine the patients' ability to fight cancer by complement dependent cytotoxicity (CDC).
The complement activation cascade that bridges between antibody binding and MAC formation is regulated by complement inhibitors that are over-expressed on tumor cells.
Target cell lysis by complement is achieved by the assembly and insertion of the membrane attack complex (MAC) composed of glycoproteins C5b through C9.
Also, recent studies show that a combination of MK and polymer further enhances the mechanical properties by complement of each other.
Tissue damage mediated by neutrophils can be initiated by complement fragments, notably C5a, which are potent stimulators of neutrophil superoxide production and adherence to coronary artery endothelium.
Hypersensitivity reactions to particulate drugs can partly be caused by complement activation and represent a major complication during intravenous application of nanomedicines.
High doses of bacteria commonly administered to experimental animals cause rapid lysis by complement.
Neurologic symptoms are mediated by complement binding anti-ganglioside antibodies [2].
All samples were treated with receptor-destroying enzyme (RDE), followed by complement inactivation the next day.
Cleavage of CFB by complement factor D liberates the Ba fragment that inhibits proliferation of B cells [45].
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