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T cells do not interact with free antigens or with antigenic sites in the surfaces of foreign microorganisms.
Instead, T cells respond only to cells bearing both a self MHC antigen and an antigenic determinant from a foreign source (i.e., from bacteria, viruses, etc.).
Thus, two stimuli are needed to trigger the proliferation and terminal differentiation of the required T-cell clones. Cytotoxic T cells respond to the combination of foreign antigen and class I MHC antigens, whereas helper T cells respond to foreign antigen and class II MHC antigens. Thus, the activities of these T cells are directed toward the body’s own cells and not to free pathogens.
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Cytotoxic T Cells:
The actions of cytotoxic T cells may be illustrated by the body’s response to viral infection (Fig. 25-17). When a virus attacks a cell, the viral nucleic acid enters the host cell and the proteins of the viral coat remain at the cell surface. Consequently, the infected cell has the proper combination of surface antigens to be recognized by cytotoxic T cells namely, class I MHC antigens and viral antigens.
Cytotoxic T cells attach to newly infected host cells, killing them (presumably through the transfer of cyto- toxins) before virus replication occurs. A number of host cells are necessarily killed by this process before the virus infection is attenuated.
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A single cytotoxic T cell may kill several host cells. Both the viral antigen and the class I MHC antigen are involved in attachment of the T cell. Still unclear is whether one T-cell receptor combines with both antigens and whether two T-cell receptors mediate the process. Figure 25-17 depicts the attachment of the two cells via a single T- cell receptor.
Helper T Cells:
Macrophages and other scavengers ingest and degrade foreign antigens, ultimately displaying their antigenic determinants at the cell surface. The combination of antigenic determinant and class II MHC antigens at the surfaces of these cells leads to the attachment and activation of helper T cells (Fig. 25-18).
Helper T cells can activate B lymphocytes and other T cells (e.g., cytotoxic and suppressor T cells). Certain helper T cells secrete lymphokines or interleukins, substances that activate macrophages and other lymphocytes. Some lymphokines attract macrophages to the site of infection. Other lymphokines prevent migration of macrophages away from the site of infection. Still other lymphokines stimulate T-cell proliferation. The net effect of lymphokine secretion is the accumulation of macrophages and lymphocytes in the region of an infection and is characterized by the inflammation that typically exists there.
Acquired Immune Deficiency Syndrome (AIDS):
No disease in recent memory has attracted so much public concern and fear as acquired immune deficiency syndrome or AIDS. The disease is caused by a virus called human T-cell lymphotropic virus-Ill or HTLV-III (HTLV-I and HTLV-II viruses in connection with cancers of the immune system). The HTLVs are retroviruses, that is, they are RNA viruses that induce their host cells to proliferate new viral genes by reverse transcription.
HTLV-III critically injures the immune system by infecting and eventually killing T cells. As a result of the progressive destruction of its T cells, the body is easily ravaged by a number of common infectious agents. In many instances, these infections would have caused little injury were there functional T-cell clones available.
Unable to battle infections in the normal manner, victims that develop a “full-blown” case of AIDS eventually succumb. In AIDS patiepts the HTLV-III virus has been shown to be present in semen as well as in the blood. Though the virus is believed to be transmitted principally through sexual contact, a number of hemophiliacs have contracted the disease as a result of receiving transfusions of infected blood. A number of infants have developed AIDS by trans placental transmission from infected mothers.
