Fig 2: NK cells recruited to the pancreas of i4F mice release lytic granules upon ligand-dependent activation. (A) Delta mean fluorescent intensity (?MFI) of the total RAE1, MULT1, ICAM1, CD155 and RAE1 expression in pancreas of WT and i4F mice treated with doxycycline (1 mg/ml) for 7 days (n=4). (B) WT and i4F mice were treated with doxycycline (1 mg/ml) for 7 days and expression levels of NK-activating ligands (Rae1, Mult1, Icam1 and CD155) in pancreatic tissue were assessed by RT-qPCR (n=5). Data in A,B are mean±s.d. *P<0.05, **P<0.01, ****P<0.0001 evaluated using the unpaired two-tailed Student's t-test. (C) Representative H&E (above) and NK1.1 staining (below) of pancreata of WT and i4F mice treated with doxycycline for 7 days (n=5). (D) Subpopulations of infiltrating NK cells in pancreas undergoing reprogramming on days 3 (D3), 5 (D5) and 7 (D7) of doxycycline treatment. Cell populations were gated on CD3-/NK1.1+ cells and stained for the indicated activation, degranulation and inhibitory markers. Correlation of NKG2A+ and CD107a+ cells includes all time points. In the box-and-whisker plots, boxes show median and upper and lower quartiles, and whiskers indicate minimum and maximum values; **P<0.01, ***P<0.001, ****P<0.0001 evaluated using one-way ANOVA (data pooled from four independent experiments).

Fig 3: NK1.1+ cell depletion enables full reprogramming and promotes teratoma formation. (A) WT mice were retro-orbitally injected with scAAV8 SFFV-hCO-O/K/S/M. A scAAV8 vector encoding GFP was additionally added as tracer. Anti-NK1.1 or isotype control antibodies were injected intraperitoneally on days -1, 3 and 5 during the first week, and then once a week until liver teratomas were palpable. (B) Survival curve upon teratoma formation in the liver. Data pooled from two independent experiments (n=9). Data are percentage of alive mice; ***P<0.001 evaluated using log-rank (Mantel-Cox) test. NT, nonteratoma; T, teratoma.