Killer Helper and Suppressor T Lymphocytes

The killer, or cytotoxic, T lymphocytes can be identified in the laboratory by a surface molecule called CD8. Their function is to destroy body cells that harbor foreign molecules. These are usually molecules from an invading microorganism, but they can also be molecules produced by the cell's genome because of a malignant transformation, or they may simply be body molecules that had never been presented before to the immune system.

In contrast to the action of B lymphocytes, which kill at a distance through humoral immunity (the secretion of antibodies), killer, or cytotoxic, T lymphocytes kill their victim cells by cell-mediated destruction. This means that they must be in actual physical contact with the victim cells. When this occurs, the killer cells secrete molecules called perforins and enzymes called granzymes. The perforins enter the plasma membrane of the victim cell and polymerize to form a very large pore. This is similar to the pore formed by the membrane attack complex of complement proteins, and results in the osmotic destruction of the victim cell. The granzymes enter the victim cell and, through the activation of caspases (enzymes involved in apoptosis—see chapter 3), cause the destruction of the victim cell's DNA.

The killer T lymphocytes defend against viral and fungal infections and are also responsible for transplant rejection reactions and for immunological surveillance against cancer. Although most bacterial infections are fought by B lymphocytes, some are the targets of cell-mediated attack by killer T lymphocytes. This is the case with the tubercle bacilli that cause tuberculosis. Injections of some of these bacteria under the skin produce inflammation after a latent period of 48 to 72 hours. This delayed hypersensitivity reaction is cell-mediated rather than humoral, as shown by the fact that it can be induced in an unexposed guinea pig by an infusion of lymphocytes, but not of serum, from an exposed animal.

The helper T lymphocytes (identified in the laboratory by the surface molecule CD4), and suppressor T lymphocytes indirectly participate in the specific immune response by regulating the responses of the B cells (fig. 15.14) and the killer T cells. The activity of B cells and killer T cells is increased by helper T lymphocytes and decreased by suppressor T lymphocytes. The amount of antibodies secreted in response to antigens is thus affected by the relative numbers of helper to suppressor T cells that develop in response to a given antigen.

Stem cell

Stem cell

Antigen

B lymphocyte

B lymphocyte

Antigen

Suppressor cells

Clone

Memory cell

Memory cell

Suppressor cells

Cytotoxic killer T lymphocyte

Antibodies

â–  Figure 15.14 The effect of an antigen on B and T lymphocytes. A

given antigen can stimulate the production of both B and T lymphocyte clones. The ability to produce B lymphocyte clones, however, is also influenced by the relative effects of helper and suppressor T lymphocytes.

Acquired immune deficiency syndrome (AIDS)

has killed approximately 22 million people worldwide. Today, more Americans have died of AIDS than were killed in World Wars I and II combined. About 36 million people worldwide are currently infected, and since AIDS has been shown to have a latency period of approximately 8 years, most will display symptoms of the disease in the near future. AIDS is caused by the human immunodeficiency virus (HIV) (see fig. 15.3), which specifically destroys the helper T lymphocytes. This results in decreased immunological function and greater susceptibility to opportunistic infections, including Pneumocystis carinii pneumonia. Many people with AIDS also develop a previously rare form of cancer known as Kaposi's sarcoma.

Current treatment for AIDS includes the use of drugs that inhibit reverse transcriptase, the enzyme used by the virus to replicate its RNA (see fig. 15.3). Recently, two different reverse transcriptase inhibitors have been combined with a protease inhibitor (protease enzymes are needed to cut viral protein into segments for assembly of the viral coat) to produce a "cocktail" that has proved to be an effective treatment. New drugs are also under development that inhibit the fusion of HIV with its victim cells by targeting the part of the glycoprotein "spokes" that protrude from the HIV particles (see fig. 15.3), which serve to anchor the virus to the plasma membrane of its victim. Hopefully, these and other new drugs will provide better treatment until a safe and effective vaccine might be developed.

The Immune System 459

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