(MASP1 and MASP2), which also activate C3 cleavage. After C5 is cleaved, all

three pathways follow the same steps [6].

b. Antibody dependent cellular cytotoxicity

In addition to recruiting the complement cascade, the Fc portion of the antibody

also mediates antibody-dependent cellular cytotoxicity (ADCC). As shown in

Figure 3.10, if a virally infected or cancer cell is bound by an antibody, the

NK cells recognize the Fc region of the antibody and this triggers NK cells to

release cytotoxic molecules such as the pore-forming perforin and the apoptosis-

inducing granzyme. The target cell is thus destroyed. It is important to note the

distinction between NK cell-mediated cytotoxicity that was discussed in the

section on innate immunity and what is being discussed here. In the previous

section, NK cells did not rely on specific antibodies for recognizing their targets,

whereas for ADCC, as the name suggests, antibodies are central to the recogni-

tion process.

FIGURE 3.9 Complement cascade. This figure is a schematic representation of the

steps involved in the three pathways that result in activation of the complement pathway.

The classical pathway is activated by the antigen-antibody complex. The binding of

lectins to mannose-rich cell surface molecules triggers the lectin pathway. The alter-

native pathway involves the formation of an activated form of a C3 fragment, by the

sequential action of proteins B, D and properidin. All three pathways converge on the

proteolytic cleavage of C5, which is followed by the formation of the membrane attack

complex.

Introduction to basic immunology

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