Molecular nature of the complement lesion.

Abstract

The principle molecular event leading to membrane perturbation by complement [C] is the assembly of the terminal 5 [human] serum C components (C5b[b fragment of C component 5]-C9) into a macromolecular C5b-9 complex on the target membrane. The ability of purified C5b-9 complexes isolated from target membranes to become reincorporated into artificial lipid vesicles was reported. The complex may be a vertically oriented, hollow, cylindrical macromolecule possessing lipid-binding regions that enable 1 terminus to penetrate into the lipid bilayer. A transmembrane pore appears to be created at the attachment site of the C5b-9 complex.