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Although humoral (antibody-mediated) immunity is an important host defense against many bacterial and viral diseases, in many other bacterial infections (especially intracellular infections such as tuberculosis) and viral infections, it is primarily the cell-mediated arm that imparts resistance and aids in recovery. Furthermore, cell-mediated immunity is important in defense against fungi, parasites, and cancers. It is also the main mechanism involved in the rejection of organ transplants. The strongest evidence for the importance of cell-mediated immunity comes from clinical situations in which its suppression (by immunosuppressive drugs or disease, e.g., acquired immunodeficiency syndrome [AIDS]) results in overwhelming infections or tumors.

The constituents of the cell-mediated immune system include several cell types: (1) macrophages, which present the antigen to T cells; (2) helper T cells, which participate in antigen recognition and in regulation (helper and suppressor) functions (see Chapter 58); (3) natural killer (NK) cells, which can inactivate pathogens; and (4) cytotoxic T cells, which can kill virus-infected cells with or without antibody. Macrophages and helper T cells produce cytokines that activate helper and cytotoxic T cells, leading to the killing of the pathogen or tumor cell.

An excellent example of cell-mediated immunity is the delayed hypersensitivity response to the tuberculin skin test in people who have been infected with Mycobacterium tuberculosis. An area of skin induration occurs at the site of the PPD injection subcutaneously. The induration is caused by the presence of macrophages and helper T cell that respond to the purified protein derivative (PPD) extracted from M. tuberculosis.

Infection with some viruses, namely, measles virus and cytomegalovirus, can suppress cell-mediated immunity against other microorganisms. In particular, measles virus infection in people infected with M. tuberculosis can result in a loss of purified protein derivative (PPD) skin test reactivity, reactivation of dormant organisms, and clinical disease. A proposed explanation for these findings is that when measles virus binds to its receptor on the surface of human macrophages, the production of interleukin-12 (IL-12) by the macrophages, which is necessary for cell-mediated immunity to occur, is suppressed.

The terms primary and secondary response are associated primarily with antibody formation as described in Chapter 60, but the timing of the T-cell response also follows the same pattern. After the initial exposure to the antigen, the specific T cell proliferates to form a small clone of cells (i.e., a primary response occurs). Then, on subsequent exposure to the antigen, the small clone expands, and many more specific T cells are formed. These cells constitute the secondary response.

Although the interactions between various cells and various cytokines are complex, the result is relatively simple: In the person with competent cellular immunity, opportunistic pathogens rarely or never cause disease, and the spread of other agents—for example, certain viruses (e.g., herpesviruses) or tumors (e.g., Kaposi’s sarcoma)—is limited. The assessment of the competence of cell-mediated immunity ...

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