NK1.1 cell depletion and adoptive transfer of TRAIL^−/− MNCs protects NEMO^Δhepa mice against ConA-mediated fulminant hepatitis. (A–C) ALT serum levels (A), H&E staining (B), TUNEL analysis, and quantification of caspase 8 (C), 6 h after 25 mg/kg ConA revealed strong attenuation of ConA hepatitis in NEMO^Δhepa mice when NK1.1 mAb was administered 40 h before insult. (D and E) mRNA levels of IFN-γ, CCL5, and IL-4 (D) and ELISA of IFN-γ and TNF (E) on serum confirmed attenuation of ConA damage in NEMO^Δhepa mice after NK1.1 mAb. (F–H) Adoptive transfer of TRAIL^−/− MNCs and liver TRAIL^−/− NK1.1⁺ cells after NK1.1 mAb protected while TRAIL^+/+ MNC transfer restored ConA injury in NEMO^Δhepa mice as shown by serum ALT (F), H&E staining (G), and ELISA (H) of IFN-γ serum levels. (I) ConA-mediated JNK activation was attenuated by NK1.1 mAb and restored by TRAIL^+/+ MNCs adoptive transfer. TRAIL^−/− cells maintained JNK inactivated. JNK1 and GAPDH act as loading control. Bars, 50 µm. All data are representative of three independent experiments. n = 4. **, P < 0.01; ***, P < 0.001 (NEMO^Δhepa vs. ConA/NEMO^Δhepa). §, P < 0.05; §§, P < 0.01; §§§, P < 0.001 (ConA/NEMO^Δhepa vs. NK1.1mAb/ConA/NEMO^Δhepa).