Adaptive immunity results either from exposure to the organ ism or vaccination (active immunity) or from receipt of preformed antibody made in another host, which is called passive adaptive immunity and affords temporary and immediate protection against an organism by providing neutralizing antibodies that can bind to a pathogen and limit its ability to interact with host cells and tissues. Passive immunization also occurs normally in the form of immunoglobulins passed through the placenta (IgG) or breast milk (IgA) from mother to child. This protection is very important during the early days of life when the infant has a reduced capacity to mount an active response. For example, immunizing mothers with the TDaP vaccine, which protects against tetanus, diphtheria, and pertussis, provides immunity not only to the mother but also to the fetus due to the passage of IgG from the mother through the placenta to the fetus. Passive immunity is relatively short-lived, lasting only a month or two, because the antibody concentration decreases fairly rapidly as the proteins are degraded. The administration of preformed antibodies can be lifesaving in certain diseases that are caused by powerful exotoxins, such as botulism and tetanus. Serum globulins, given intravenously, are a prophylactic measure in patients with hypogammaglobulinemia or bone marrow transplants. In addition, they can mitigate the symptoms of certain diseases such as hepatitis caused by hepatitis A virus.
Active adaptive immunity is protection based on exposure to the organism in the form of overt disease, subclinical infection (i.e., an infection without symptoms), or a vaccine. This protection has a slower onset but longer duration than passive immunity. The primary response usually takes 7–10 days for the antibody to become detectable. An important distinction between active and innate immunity is that the former has a memory component such that upon subsequent encounters with the same antigen, there is a rapid response that includes production of antigen-specific antibodies from memory B cells and/or activation of memory T cells. Active immunity is mediated by both antibodies and T cells:
(1) Antibodies protect against organisms by a variety of mechanisms—neutralization of toxins, lysis of bacteria in the presence of complement, opsonization of bacteria to facilitate phagocytosis, and interference with adherence of bacteria and viruses to cell surfaces.
Because antibodies, especially IgG, rise to a protective level slowly (∼7–10 days after the first encounter), they do not play a major role in combating primary infection but rather protect against a second infection by that organism.
(2) T cells mediate a variety of reactions, including cytotoxic destruction of virus-infected cells, activation of macrophages, and delayed hypersensitivity. T cells, especially Th-1 cells, and macrophages are the main host defense against mycobacteria such as M. tuberculosis and systemic fungi such as Histoplasma and Coccidioides. T cells also help B cells to produce antibody against many antigens.
Table 1 describes the essential host defense mechanisms against bacteria, which include both humoral immunity against bacteria and exotoxins, and cell-mediated immunity against several intracellular bacteria.
Table1. Essential Host Defense Mechanisms Against Bacteria
