T-bet suppresses the expression of immature NK cell-defining genes.

Neonatal ILC1-like cells are functionally immature but have the unique potential to generate NK cells characterized by downregulation of NKG2A and a highly diverse KIR receptor repertoire.

RUNX2 plays an important role in human NK cell biology by driving differentiation, inhibiting cytokine production, and inducing a tissue-resident phenotype, which has implications for improving NK cell therapy for cancer patients.

Toxoplasma gondii infection leads to conversion of natural killer cells into cells resembling innate lymphoid cells, group 1, that circulate widely, disrupting current notions suggesting that these cells have distinct lineages.

Human NK cells engineered to express a PD-L1 chimeric antigen receptor can control murine and human tumors and reduce myeloid cells expressing high levels of PD-L1.

Extracellular vesicles derived from natural killer cells contain a specific repertoire of microRNAs that promote Th1 responses.

Antitumor (natural killer) NK cell responses are negatively regulated by interactions between NK cells and endogenous NKG2D ligands constitutively expressed on lymph node endothelial cells and super-induced on tumor-associated endothelium.

During pathogen infection, natural killer cells require hypoxia-inducible factor-1α for optimal metabolism to prevent apoptosis, thereby reducing viral load and protecting against morbidity.

Natural killer cells that were commonly thought to circulate around the body can actually reside in distinct tissues, such as in the liver, skin or uterus, and do not re-circulate.

Metabolic abnormalities in hepatocytes cause the alteration of transcriptional profile and function of immune cells in the tissue microenvironment.