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Johnstone CA Jr, Travers P, Walport M, et al."The Immune System in Health and Disease.".Fifth Edition.a Garland Science publication.
Most of the bacteria that cause infectious diseases in humans multiply in the extracellular spaces of the body, and they spread from cell to cell through the extracellular fluids.Humoral immunity protects extracellular spaces, in which antibodies made by B cells destroy extracellular microorganisms and prevent intracellular infections from spreading.Antigens come into contact with B cells, triggering their differentiation into antibody-secreting plasma cells (Fig. 9.1).In the context of B-cell activation, the term 'helper T cell' is generally used to refer to cells from the TH2 class of CD4 T cells (see Chapter 8). However, a subset of TH1 cells can also be helpful.In this chapter, helper T cells will mean any armed effector CD4 T cell that can activate a B cell.These T cells also control isotype switching, as well as somatic hypermutation of antibody variable V-region genes, processes described in Chapter 4.
By way of antibody molecules, plasma cells mediate the humoral immune response.In addition to signaling B cells, antigens that bind to B-cell antigen receptors are internalized and processed to form peptides that activate armedhelper.
Antibodies contribute to immunity in three different ways (see figure 9.1).Viruses and intracellular bacteria adhere to specific molecules on the target cell surface to enter.The pathogen is neutralized by antibodies that bind to the pathogen.Immune neutralization is also important in preventing bacteria's toxins from entering cells.The main way antibodies prevent bacteria from multiplying outside of cells is by facilitating the uptake of the pathogen by phagocytic cells that are specialized in destroying the ingested bacteria.Antibodies can do this in two ways.A pathogen coating is recognized by the Fc receptors on phagocytic cells which bind to the antibody constant C region (see Section 4-18).Optionizing a pathogen's surface makes it more resistant to phagocytosis.The complement system, which was outlined in Chapter 2, is activated by antibodies binding to the surfaces of pathogens.By activating the complement system, complement proteins adhere to pathogen surfaces and bind their complement receptors, opsonizing them.Additionally, complement components can trigger phagocytic cells to migrate to the site of infection by recruiting phagocytic cells, and the terminal components of complement can lyse certain microorganisms directly by forming pores in their membranes. The particular effector mechanisms used in a particular response depend on the isotype or class of antibodies produced.
It will be discussed in this chapter how helper T cells and B cells interact to produce antibodies, the affinity maturation of this antibody response, isotype switching, which confers functional diversity, and the generation of memory B cells that provide long-lasting immunity against reinfection.The rest of this chapter details how antibodies contain and eliminate infections.
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