Natural killer cell-produced IFN-γ and TNF-α induce target cell cytolysis through up-regulation of ICAM-1.

NK cells control tumor and virus-infected cells through releasing cytotoxic granules and proinflammatory cytokines. IFN-γ and TNF-α secretions and cytotoxicity are regarded as two distinct functions of NK cells with little synergy in between as results of early association of the two functions with distinct subsets of NK populations and of the studies showing target cells developing NK resistance upon IFN-γ treatment. Here, we show that IFN-γ and TNF-α synergistically enhance NK cell cytotoxicity through NF-κB-dependent up-regulation of ICAM-1 expression in target cells, thereby promoting their conjugate formation with NK cells.

Crystal structure of human natural cytotoxicity receptor NKp30 and identification of its ligand binding site.

Natural killer (NK) cells are a group of innate immune cells that carry out continuous surveillance for the presence of virally infected or cancerous cells. The natural cytotoxicity receptor (NCR) NKp30 is critical for the elimination of a large group of tumor cell types. Although several ligands have been proposed for NKp30, the lack of a conserved structural feature among these ligands and their uncertain physiological relevance has contributed to confusion in the field and hampered a full understanding of the receptor.

Crystal structure and oligomeric state of the RetS signaling kinase sensory domain.

The opportunistic pathogen Pseudomonas aeruginosa may cause both acute and chronic-persistent infections in predisposed individuals. Acute infections require the presence of a functional type III secretion system (T3SS), whereas chronic P. aeruginosa infections are characterized by the formation of drug-resistant biofilms.