Type I IFN promotes NK cell expansion during viral infection by protecting NK cells against fratricide

Madera, Sharline; Rapp, Moritz; Firth, Matthew A.; Beilke, Joshua N.; Lanier, Lewis L.; Sun, Joseph C.

All mice used in this study were bred and maintained at Memorial Sloan Kettering Cancer Center (MSK CC) in accordance with all guidelines of the Institutional Animal Care and Use Committee. This study used the following mouse strains, all on the C57BL/6 genetic background: C57BL/6 (CD45.2; The Jackson Laboratory), B6.SJL (CD45.1; Taconic), Ifnar1 −/− (Müller et al., 1994) , Stat1 −/− (Meraz et al., 1996) (Gazit et al., 2006) , Prf1 −/− (The Jackson Laboratory), and R26 DTA (The Jackson Laboratory). NKp46 Cre x R26 DTA mice were generated at MSK CC. Adoptive transfer studies and the generation of mixed bone marrow chimeric mice were performed as previously described (Sun et al., 2009) . Bone marrow chimeric mice were infected by i.p. injections of 7.5 × 10 3 PFU of salivary gland-derived Smith strain MCMV. Mice used in adoptive transfer studies were infected with 7.5 × 10 2 PFU of MCMV. Newborn Ly49H-deficient mice were infected with 2 × 10 3 PFU of MCMV. LCMV infection was performed as described previously (Sun et al., 2004) . In vivo blockade of NKG2D signaling was accomplished by i.p. injection of anti-NKG2D (clone CX5; 200 µg/mouse) on day 0 of LCMV infection.