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Figure 15.8 Membrane Attack Complex of Complement (MAC) (a) The MAC is formed after C5b,C6,and C7 combine into a complex on the cell surface of bacteria or other foreign cells.This complex, together with C8, causes changes in C9, allowing it to polymerize with the complex and form a MAC.The MAC forms a pore in the membrane, resulting in lysis of the cell. (b) An electron micrograph of MACs; each dark dot is a MAC.

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Figure 15.8 Membrane Attack Complex of Complement (MAC) (a) The MAC is formed after C5b,C6,and C7 combine into a complex on the cell surface of bacteria or other foreign cells.This complex, together with C8, causes changes in C9, allowing it to polymerize with the complex and form a MAC.The MAC forms a pore in the membrane, resulting in lysis of the cell. (b) An electron micrograph of MACs; each dark dot is a MAC.

protein in the cascade, and so on. Generally, activation involves splitting the protein into two parts, each of which then carries out a specific function. Stringent mechanisms operate to control the complement system at various points.

The major complement components have each been given a number along with the letter C, for complement. The nine major components, C1 through C9, were numbered in the order in which they were discovered and not the order in which they react. When one of these components is split into two molecules, a lowercase letter is added to the name. For example, the activation of C3 splits it into C3a and C3b. Note that C3 spontaneously splits into C3a and C3b even when the complement system has not been activated, but does so at a very low rate; this spontaneous hydrolysis allows enough C3b to be present to potentially trigger the alternative pathway of complement activation. ■ hydrolysis, p. 25

Activation of the complement system eventually leads to three major protective outcomes:

■ Inflammation. The complement components C3a and C5a induce changes in endothelial cells, which line the blood vessels, and in mast cells. These effects contribute to the vascular permeability associated with inflammation. C5a is a potent chemoattractant, drawing phagocytes into the area where complement was activated.

■ Lysis of foreign cells. Complexes of C5b, C6, C7, C8, and multiple C9 molecules, spontaneously assemble in the membranes of cells, forming doughnut-shaped structures each called a membrane attack complex (MAC) (figure 15.8). This creates pores in that membrane, disrupting the integrity of the cell. Note that the membrane attack complex has little effect on

Gram-positive bacteria because their peptidoglycan layer prevents the complement components from reaching their cytoplasmic membrane. The outer membrane of Gram-negative bacteria, however, renders them susceptible.

■ Opsonization. The complement protein C3b binds to foreign material; phagocytes more easily "grab'' particles coated with C3b because phagocytic cells have receptors for the molecule on their surface. The material that C3b has coated is said to be opsonized (which means "prepared for eating"); compounds such as C3b that can opsonize material are called opsonins. Opsonized material may be viewed as carrying a giant "eat me" sign that can be read by phagocytes. Our own cells are protected from the effects of C3b because our membranes contain regulatory molecules, leading to the inactivation of C3b when it binds. C3a and C5a cause phagocytes to produce more receptors for C3b on their surfaces. They also directly stimulate metabolic activity of phagocytes.

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