All mice used in this study were bred and maintained at Memorial Sloan Kettering Cancer Center (MSKCC) 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 (
link)),
Stat1−/− (Meraz et al., 1996 (
link)),
Klra8−/− (Ly49H deficient; Fodil-Cornu et al., 2008 (
link)), Nkp46
iCre (referred to as NKp46
Cre; Narni-Mancinelli et al., 2011 (
link)),
B2m−/− (Taconic),
Rag2−/−Il2rg−/− (Taconic),
Ncr1gfp/gfp (Gazit et al., 2006 (
link)),
Prf1−/− (The Jackson Laboratory), and R26
DTA (The Jackson Laboratory). NKp46
Crex R26
DTA mice were generated at MSKCC. Adoptive transfer studies and the generation of mixed bone marrow chimeric mice were performed as previously described (Sun et al., 2009 (
link)). 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 (
link)). 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.
Madera S., Rapp M., Firth M.A., Beilke J.N., Lanier L.L, & Sun J.C. (2016). Type I IFN promotes NK cell expansion during viral infection by protecting NK cells against fratricide. The Journal of Experimental Medicine, 213(2), 225-233.