The third function of antibodies is complement activation. In Section 1-2 we briefly mentioned Bordet’s discovery of complement as a serum factor that ‘complements’ the activities of antibodies. Complement can be activated by microbial surfaces even without the help of antibodies, which leads to the covalent deposition of certain complement proteins onto the bacterial surface. But when an antibody binds first to the bacterial surface, its constant region provides a platform that is much more efficient in complement activation than the left panels show antibodies binding to and neutralizing a bacterial toxin, thus preventing it from interacting with host cells and causing pathology. unbound toxin can react with receptors on the host cell, whereas the toxin:antibody complex cannot. Antibodies also neutralize complete virus particles and bacterial cells by binding and inactivating them. the antigen:antibody complex is eventually scavenged and degraded by macrophages. Antibodies coating an antigen render it recognizable as foreign by phagocytes (macrophages and neutrophils), which then ingest and destroy it; this is called opsonization. the center panels show opsonization and phagocytosis of a bacterial cell. Antibody first binds to antigens (red) on the bacterial cell through the variable regions. then the antibody’s Fc region binds to Fc receptors (yellow) expressed by macrophages and other phagocytes, facilitating phagocytosis. the right panels show activation of the complement system by antibodies coating a bacterial cell. Bound antibodies form a platform that activates the first protein in the complement system, which deposits complement proteins (blue) on the surface of the bacterium. this can lead in some cases to formation of a pore that lyses the bacterium directly. more generally, complement proteins on the bacterium can be recognized by complement receptors on phagocytes; this stimulates the phagocytes to ingest and destroy the bacterium. thus, antibodies target pathogens and their toxic products for disposal by phagocytes.
microbial activation alone. Thus, once antibodies are produced, complement activation against a pathogen can be substantially increased.
Certain complement components that are deposited on the bacterial surface can directly lyse the membranes of some bacteria, and this is important in a few bacterial infections (see Fig. 1.28, right panels). The major function of complement, however, is to enable phagocytes to engulf and destroy bacteria that the phagocytes would not otherwise recognize. Most phagocytes express receptors that bind certain complement proteins; called complement receptors, these receptors bind to the complement proteins deposited onto the bacterial surface and thus facilitate bacterial phagocytosis. Certain other complement proteins also enhance the phagocytes’ bactericidal capacity. The end result is that all pathogens and free molecules bound by antibody are eventually delivered to phagocytes for ingestion, degradation, and removal from the body (see Fig. 1.28, bottom panels). The complement system and the phagocytes that antibodies recruit are not themselves antigen-specific; they depend upon antibody molecules to mark the particles as foreign.
the effector mechanisms of immunity.
1-21 T cells orchestrate cell-mediated immunity and regulate B-cell responses to most antigens.
Some bacteria and parasites, and all viruses, replicate inside cells, where they cannot be detected by antibodies, which access only the blood and extracellular space. The destruction of intracellular invaders is the function of the T lymphocytes, which are responsible for the cell-mediated immune responses of adaptive immunity. But T lymphocytes participate in responses to a wide variety of pathogens, including extracellular organisms, and so must exert a wide variety of effector activities.