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.

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.

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

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

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

SARS-CoV-2 host-shutoff inhibits innate NK surveillance by suppressing activating ligands, however ADCC provides a potent NK stimulus that is mediated by antibodies targeting Nucleocapsid, ORF3a, and Membrane, with those targeting Spike being significantly weaker.

Mucosal-associated invariant T cells, an emerging member of the innate-like T cells abundant in humans bridging the innate and the adaptive immunity, could be exploited as a novel tool for cancer immunotherapy through cell reprogramming.

Tissue-resident natural killer cells are important mediators of CD8 T responses in human cancers and these cells can be harnessed to increase immunity against pancreatic ductal adenocarcinoma.

Innate lymphoid cells type 1 suffice to induce hallmarks of alopecia areata phenotype in organ-cultured human scalp hair follicles ex vivo and in human scalp skin xenotransplants in vivo, suggesting that these cells play a role in early AA pathogenesis.