Signals For Deactivation And Apoptosis

As one of the immune system's most powerful front-line defences, NK cells must be tightly regulated to prevent attacks on healthy cells or initiation of excessive immune responses. Several mechanisms serve to provide the needed regulation.

Once an NK cell kills its target it may go on to kill other targets, become inactivated, or undergo activation-induced cell death (AICD). Although the NK cell's ability to initiate signals in response to activating and inhibitory ligands on a target cell does not depend on its interactions with activating and inhibitory ligands on previously encountered cells, the NK cell's survival may nevertheless be influenced by its previous activation. For example, as part of their activation, NK cells upregulate Fas (in addition to FasL) [81,82]. Thus, like their targets that express Fas, NK cells are susceptible to killing through this death receptor pathway. The Fas receptor is upregulated by signaling through FcR and possibly other receptors [81,83], resulting in a suicide mechanism.

Many of the signals that initiate the NK cell's cytotoxic functions may also result in the cell's eventual death. For example, signaling through MAP kinases has been implicated in regulating cell survival and apoptosis in lymphocytes. Similarly, IL-2 not only activates NK cells; it also increases the likelihood that they will die by AICD [84]. These self-destructive mechanisms act as controls on NK cells.

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