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Specifically, we show that human natural killer cells have the ability to produce IGF-1 and that differential endogenous IGF-1 expression leads to disparate cytotoxicity in human primary natural killer cells

The specific mechanism may involve the release of VacA by HP, which in turn induces membrane pore formation that results in energy loss from the mitochondria, and affects the formation of mTORC1 complex, with the onset of autophagy (Figure 1)

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