The paradox of NKp46+ natural killer cells: drivers of severe hepatitis C virus-induced pathology but in-vivo resistance to interferon α treatment.

Detailed ex-vivo phenotypic analyses, without restimulation, confirm that intrahepatic NK cells have been activated in situ indicated by a highly significant downregulation in CD16 and NKp30 in HCV and CLD groups (p < 0.0001; figure 2 B,C); downregulation in NKG2D expression (HCV cohort only p=0.01; figure 2 D); and significantly increased expression of IFN-γ and CD107a with decreased intracellular granzyme B (p<0.006; figure 2 F–I).

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