Activation of hepatic natural killer cells and control of liver-adapted lymphoma in the murine model of cytomegalovirus infection.

Hematopoietic stem cell transplantation (HSCT) is a promising therapeutic option against hematopoietic malignancies. Infection with cytomegalovirus (CMV) and tumor relapse are complications that limit the success of HSCT. In theory, CMV infection can facilitate tumor relapse and growth by inhibiting "graft take" and reconstitution of the immune system or by inducing the secretion of tumor cell growth-promoting cytokines. Conversely, one can also envisage an anti-tumoral effect of CMV by cytopathic/oncolytic infection of tumor cells, by inducing the secretion of death ligands for tumor cell apoptosis, and by the activation of systemic innate and adaptive immunity. Here we will briefly review the current knowledge about tumor control in a murine model of CMV infection and liver-adapted B cell lymphoma, with a focus on a putative implication of CD49(+)NKG2D(+) hepatic natural killer cells.