Which molecule is most effective in preventing bystander lysis of RBCs during complement activation?

Which molecule is most effective in preventing bystander lysis of RBCs during complement activation?

• A. C1-INH
• B. Factor H
• C. DAF
• D. Factor B

Answer: (C)

The main concept is how host cells are protected from damage during complement activation by surface regulators that shut down the cascade on those cells. The molecule that best prevents bystander lysis on red blood cells is the decay-accelerating factor. It sits on the cell surface and directly disrupts the C3 convertases that would amplify the cascade: it binds to C4b and C2a to inactivate the classical/lectin pathway convertase, and it promotes dissociation of the alternative pathway C3 convertase (C3bBb). By accelerating the decay of these convertases, it lowers C3 breakdown and downstream C5 convertase formation, leading to less C5b-9 membrane attack complex deposition on the host cell. That direct, on-cell regulation is why DAF is most effective at preventing bystander lysis of RBCs during complement activation. C1-INH blocks initiation of the classical pathway but doesn’t rapidly dissociate surface convertases; Factor H helps regulate the alternative pathway but works more broadly and not as directly at the cell surface; Factor B is a component that promotes convertase formation, not prevents it.

The main concept is how host cells are protected from damage during complement activation by surface regulators that shut down the cascade on those cells. The molecule that best prevents bystander lysis on red blood cells is the decay-accelerating factor. It sits on the cell surface and directly disrupts the C3 convertases that would amplify the cascade: it binds to C4b and C2a to inactivate the classical/lectin pathway convertase, and it promotes dissociation of the alternative pathway C3 convertase (C3bBb). By accelerating the decay of these convertases, it lowers C3 breakdown and downstream C5 convertase formation, leading to less C5b-9 membrane attack complex deposition on the host cell. That direct, on-cell regulation is why DAF is most effective at preventing bystander lysis of RBCs during complement activation.

C1-INH blocks initiation of the classical pathway but doesn’t rapidly dissociate surface convertases; Factor H helps regulate the alternative pathway but works more broadly and not as directly at the cell surface; Factor B is a component that promotes convertase formation, not prevents it.