Final answer:
The C3bBb complex on a human cell-surface can be disrupted by Decay Accelerating Factor (DAF) or Membrane Cofactor Protein (MCP), with the direct answer being e. A & C. DAF and MCP are part of the regulatory mechanisms that prevent complement-mediated damage to host cells.
Step-by-step explanation:
The action of either Decay Accelerating Factor (DAF) or Membrane Cofactor Protein (MCP) can rapidly disrupt the formation of C3bBb on a human cell-surface. Thus, the direct answer is e. A & C.
C3bBb is a complex that forms part of the complement system, an essential aspect of the innate immune response. It functions as a C3 convertase in the alternative pathway of complement activation. However, human cells have regulatory mechanisms to protect themselves from being targeted by their own immune system. DAF and MCP are two such regulators. When C3bBb is formed on a human cell-surface, it can be rapidly disrupted by the actions of Decay Accelerating Factor (DAF) and Membrane Cofactor Protein (MCP). DAF prevents the formation of C3 convertase, which is necessary for the stability of C3bBb. MCP helps in the dissociation of C3 convertase. DAF acts by dissociating the Bb from C3b, thereby disrupting the convertase, while MCP serves as a cofactor for factor I, which cleaves C3b into its inactive form. This activity prevents the formation of the membrane-attack complex (MAC) on self-cells, which would otherwise lead to cell lysis.
Note that Properdin (Factor P) stabilizes C3bBb, thus aiding in the continuation of the complement pathway, rather than disrupting it.