Loss of DNAM-1 ligand expression by acute myeloid leukemia cells renders them resistant to NK cell killing.

ABSTRACT: Acute myeloid leukemia (AML) is associated with poor natural killer (NK) cell function through aberrant expression of NK-cell-activating receptors and their ligands on tumor cells. These alterations are thought to promote formation of inhibitory NK-target cell synapses, in which killer cell degranulation is attenuated. Allogeneic stem cell transplantation can be effective in treating AML, through restoration of NK cell lytic activity. Similarly, agents that augment NK-cell-activating signals within the immunological synapse may provide some therapeutic benefit. However, the receptor-ligand interactions that critically dictate NK cell function in AML remain undefined. Here, we demonstrate that CD112/CD155 expression is required for DNAM-1-dependent killing of AML cells. Indeed, the low, or

SUBMITTER: Kearney CJ 

PROVIDER: S-EPMC5007960 | biostudies-literature | 2016 Aug

REPOSITORIES: biostudies-literature