However, despite the lack of receptor expression on NK cells and the lack of responsiveness of these cells to IFN-λ in vitro, a model of acute endotoxemia shows that NK cells derived from IFNLR1−/− spleens have defective IFN-γ production, and IFNLR1−/− mice are partially protected from lethal doses of LPS or in a CLP model of sepsis, in a IFN-γ-dependent manner. Here, IFNLR1 is linked to serum lipopolysaccharide activity.