Keeping NK cells in highly regulated antiviral warfare

Abstract

Natural killer (NK) cells use multiple mechanisms to defend against viral infections, and different stimuli can activate these antiviral effects. When engaged, receptors for innate cytokines produced during infections and for ligands on target cells can both induce NK cell cytotoxicity and the production of cytokines. These stimuli use different classes of intracellular signaling pathways to elicit the overlapping responses. What is the advantage of using different roads to the same ends? One answer might be in the nature of the alternative regulatory pathways that are in place to control the respective stimuli. A model of flexibility in accessing NK cell function, in the context of negative regulation of particular intracellular signaling pathways, is proposed here.