Complement membrane attack complex

Antibody-mediated complement activation leads to MAC deposition on the surface of infected cells.

These fluid phase complexes do not bind to cell membranes and are ultimately scavenged by clusterin and vitronectin, two regulators of complement.

This junction alters the configuration of the protein molecules exposing a hydrophobic site on C7 that allows the C7 to insert into the phospholipid bilayer of the pathogen.

C8 alpha-gamma induces the polymerization of 10-16 molecules of C9 into a pore-forming structure known as the membrane attack complex.

A rare condition, paroxysmal nocturnal haemoglobinuria, results in red blood cells that lack CD59.

Inhibition of MAC has been shown to reduce inflammation and neuroaxonal loss at 72 hours post-Traumatic Brain Injury (TBI) event, potentially preventing neurological damage, especially in cases with acquired sepsis or respiratory failure.