Characterization of the role of TCRγδ in NK cell accumulation during viral liver inflammation

Abstract

Polyinosinic–polyctidylic acid (Poly I:C) is a viral RNA mimic that can induce immune responses similar to that seen during viral infection. Although poly I:C administration into mice is associated increased NK cell infiltrates in the liver, the mechanisms underlying increased hepatic NK cell accumulation in response to poly I:C administration are incompletely defined. In the current study, we have identified a novel and important role for γδT cells in driving the accumulation and activation of NK cells in the liver during poly I:C-mediated viral liver infection. Specifically, NK cell accumulation but not activation in γδT cell deficient mice following poly I:C administration was significantly attenuated in comparison to that seen in poly I:C-treated wildtype mice. The ability of γδT cells to promote NK cell accumulation and activation in the liver may be virus-specific since NK cell accumulation in the liver was not altered by TCRγδ deficiency following adenovirus administration.