Finally, to examine if sepsis modulated the ability of subsets of NK-cells to produce effector cytokines (e.g. IFN-γ), Sham or CLP-derived splenocytes were stimulated with plate bound stimulatory antibodies to different activating NK-cell receptors (NK1.1, NKp46, Ly49D, or Ly49H) or control IgG antibodies [73], and we assessed IFN-γ production and upregulation of GzmB for cells expressing the receptor stimulated with its agonistic/specific Ab compared to IgG control. This evidence concerns the gene NCR1 and Sepsis.