FIGURE 23-7 Interplay of innate and adaptive immune responses to a bacterial pathogen. Once a bacterium breaches the host’s mechanical and chemical defenses, the bacterium is exposed to components of the complement cascade, as well as to innate immune-system cells that confer immediate protection (step 1). Various inflammatory proteins induced by tissue damage contribute to a localized inflammatory response. Local destruction of the bacterium results in the release of bacterial antigens, which are delivered, via the afferent lymphatic vessels that drain the tissue, to the lymph nodes (step 2). Dendritic cells acquire antigen at the site of infection, become migratory, and move to the lymph nodes, where they activate T cells (step 3). In the lymph nodes, antigen-stimulated T cells proliferate and acquire effector functions, including the ability to help B cells (step 4), some of which may move to the bone marrow and complete their differentiation into plasma cells there (step 5). In later stages of the immune response, activated T cells provide additional assistance to antigen-experienced B cells to yield plasma cells that secrete antigen-specific antibodies at a high rate (step 6). Antibodies produced as a consequence of the initial exposure to the bacterium act in synergy with complement to eliminate the infection (step 7), should it persist, or afford rapid protection in the case of re-exposure to the same pathogen.