Though adaptive NK cells do not possess antigen specificity, they exhibit dynamic expansions of defined cell subsets, increased proliferation and long-term persistence for up to 3 months in vivo, high IFN-γ production, potent cytotoxic activity upon ex vivo restimulation, and protective memory responses.

[1] Persistent adaptive NK populations have been reported during viral infection, contact hypersensitivity reactions, and after stimulation by pro-inflammatory cytokines or activating receptor pathways.

[6] HCMV-associated NKG2C+ adaptive NK cells and IL-12/15/18 pre-activated NK cells have been detected to have an epigenetic imprint, for instance, the demethylated CNS1 region of the IFNG gene, which in turn can lead to a remarkable stability of the IFN-γ-producing phenotype even after adoptive transfer.

After stimulation through CD16 ligation adaptive NK cells produce large amounts of IFN-γ and also extensively proliferate.

It had been indicated similar or reduced degranulation of CD107a as compared to cNK cells after CD16 ligation or stimulation with antibody-coated tumor targets.

[11] Adaptive NK cells can mediate the enhanced antitumor effects, that may be due to their increased cytotoxicity, high IFN-γ production capacity, and persistence in large numbers in the host.

[11] KIR-ligand mismatch has a beneficial effect on the alloreactivity of donor NK cells against recipient leukemia.