Polymicrobial sepsis influences NK-cell-mediated immunity by diminishing NK-cell-intrinsic receptor-mediated effector responses to viral ligands or infections
Fig 9
Sepsis-induced loss of DAP12 is causal in NK-cell-intrinsic impairments.
(A) Experimental Design. BM chimeras containing mCherry+ control (Ctrl) vector or DAP12-overexpression (DAP12-OE) were generated. Following reconstitution mice underwent Sham or CLP surgery. 2 days after surgery IFN-γ production in response to DAP12-dependent receptor (Ly49H and Ly49D) stimulation was assessed. (B) Representative flow plot of mCherry expression on WT, Ctrl, and DAP12-OE Ly49H+ splenic NK-cells, numbers indicate frequency of mCherry+ cells. Frequency of IFN-γ+ of stimulated receptor+ NK-cells from Sham or CLP mice after 8 hrs stimulation with plate bound control (IgG), αLy49H (C), or αLy49D (D) antibody. Data are representative from 2 independent experiments with 2–3 mice per group. Numbers above bars show fold change between groups. * p<0.05. Error bars represent the standard error of the mean.