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.

Viral infection can induce NKG2D ligand expression through the action of virally encoded histone deacetylase (HDAC) inhibitors, which release HDAC mediated repression of NKG2D ligands.

Macrophages respond to elevated levels of CSF-1 in tumor micro-environments by expressing a ligand for the NKG2D immunoreceptor.

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.

Rodent herpesvirus Peru overcomes NK ‘missing-self’ killing using a non-classical MHC-I like protein resistant todownregulation by its own ubiquitin ligase that potently sabotages antigen presentation to T-cells.

Forward genetic screening has provided insight into the molecular mechanisms and stress pathways that promote tumor cell recognition by natural killer cells.

A mouse model of atopic dermatitis provides mechanistic evidence for an association between allergic disease and skin cancer.

The well-established oncogene IMP3 impairs the interaction between cancer cells and the immune system.

Similar to T cell exhaustion, natural killer cell dysfunction in chronic hepatitis B patients results from deregulated calcium pathway.

The human cytomegalovirus US12 gene family work co-operatively to degrade large numbers of immune ligands and prevent recognition by natural killer cells.