Question

The formation of the C3 convertase is a key step in complement activation that occurs in all three complement pathways. This enzyme cleaves C3 in blood plasma, leading to a conformational change in the C3b fragment that exposes its reactive

thioester group. The activated C3b is potentially harmful to the host, if it becomes covalently attached to a host cell, rather than to the surface of a pathogen. This deleterious outcome is largely avoided by:

A. The inability of active C3b to diffuse away in the blood plasma.
B. The inability of active C3b to covalently attach to the membranes of eukaryotic
cells.
C. The rapid hydrolysis of active C3b in solution, rendering it inactive.
D. The tight binding of active C3b to the C3 convertase.
E. The ability of active C3b to recruit phagocytic cells.

Answer 1

The potentially harmful effects of activated C3b on host cells are largely avoided due to the rapid hydrolysis of active C3b in solution, rendering it inactive and preventing its integration into healthy host cell membranes.

Step-by-step explanation:

The deleterious outcome of activated C3b binding to host cells, rather than to the surface of a pathogen, is largely avoided by C. the rapid hydrolysis of active C3b in solution, rendering it inactive.

This is crucial because although C3b is an important component in the complement system, responsible for opsonization and the initiation of the membrane-attack complex (MAC), it must be regulated to prevent damage to host cells.

The physiological mechanism that protects host cells involves the rapid hydrolysis of C3b when it is not immediately bound to a pathogen surface, thus preventing its integration into healthy host cell membranes.

Answer 2

The rapid hydrolysis of activated C3b in solution prevents it from binding to and damaging host cells, thus ensuring that the complement system targets only pathogens and not the body's own tissues.

Step-by-step explanation:

The question pertains to the mechanism by which host cells are protected from the potentially harmful effects of activated C3b during the complement activation process. In all three pathways of complement activation—the classical pathway, the alternative pathway, and the lectin pathway—the formation of C3 convertase is crucial as it cleaves the C3 molecule into C3a and C3b. The C3b fragment, which is then able to bind covalently to pathogen surfaces, has a reactive thioester group that must be controlled to avoid damage to host cells.

In this context, the correct answer is C: The rapid hydrolysis of active C3b in solution, renders it inactive. This mechanism ensures that the activated C3b that does not immediately find a pathogenic target becomes hydrolyzed and thereby inactivated before it can bind to and potentially damage host cells. Moreover, endogenous regulatory proteins present in the host's body help to prevent the binding of complement components like C3b to host cells, allowing for a distinction between self and non-self cells.

I choose only one option: the rapid hydrolysis of active C3b in solution, rendering it inactive, which is essential for preventing the attachment of C3b to host cells, thus avoiding host tissue damage during the immune response.