During an active infection, various types of immune cells become activated and begin to destroy pathogens and infected host cells. These include macrophages, natural killer cells, and helper T cells. When the infection is a virus or other intracellular pathogen, a particular type of immune response, called a cell-mediated response, is activated. This type of immune response activates cytotoxic T cells, which are capable of targeting and killing infected host cells with a high degree of specificity.
When a naïve cytotoxic T cell is activated, it begins to undergo clonal expansion, which means that the cell begins dividing to produce more cells exactly like it. At the end of the clonal expansion phase, the immune system is then armed with millions of new, active cells, all of which have receptors that are specific for the pathogen invading the body. This specificity is important because without it, the killer T cells would attack healthy cells as well as infected ones.
Newly active cells begin to roam the body, migrating to the site of infection. When it encounters infected cells, a cytotoxic T cell will lock on to its target and release destructive chemicals called perforin, granulysin, and granzymes. The perforin tears tiny holes in the target cell’s membrane, allowing the other chemicals to enter. Granzymes and granulysin are enzymes that, upon entering the target cell, start a cascade of chemical reactions that eventually cause the cell to die.
Cytotoxic T cells are capable of killing tumor cells as well as infected cells. This is because tumor cells often become coated in abnormal proteins that are not produced by healthy cells. Any cytotoxic T cells with receptors that specifically recognize the abnormal proteins can become activated to destroy tumor cells, thereby helping to reduce the likelihood that cancer might develop. Some experimental cancer treatments, therefore, attempt to activate the body’s immune response to its own cancer cells, but the success rate of these types of treatments are highly variable.
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