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.

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.

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

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

Chronic engagement of Natural killer cell inhibitory receptors by MHC-I molecules maintains a high activity of the mTOR pathway allowing subsequent amplification of signaling through activating receptors upon acute stimulation.

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

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

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

mTORC1 and mTORC2 play a central role in the development of natural killer (NK) cells.

While acute senescence of decidualizing cells drives the inflammatory response underpinning uterine receptivity, subsequent clearance by activated natural killer cells transiently rejuvenates the cycling endometrium, enabling transition into a gestational tissue upon embryo implantation.