{'fraction_non_alphanumeric': 0.034203420342034205, 'fraction_numerical': 0.0063006300630063005, 'mean_word_length': 5.2824858757062145, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
NKG2D‐Rea1 recognition between NK cells and Kupffer cells in a novel NK cell‐dependent fulminant hepatitis

Increasing evidences suggest the contribution of NK cells in the pathogenesis of human hepatitis, but the mechanisms remain to be further investigated. In this study, we demonstrate that poly I:C can induce severe liver injury in D‐galactosamine (D‐GalN) sensitized mice. Further experiments show that the liver injury induced by poly I:C/D‐GalN depends on the cooperation between NK cells and Kupffer cells. poly I:C/GalN induce Kupffer cells to produce TNF‐¦Á and to express the retinoic acid early inducible‐1 (RAE 1) proteins, which then stimulates NK cells to produce IFN‐¦Ã via NKG2D‐RAE 1 interaction. The NK‐derived IFN‐¦Ã and Kupffer cells‐derived TNF‐¦Á induce severe liver injury via synergic effects. These results suggest that NK cells and Kupffer cells have a synergic effect on liver injury and provide the first in vivo evidence that NKG2D/ligand interaction are involved in the cooperation between NK cells and macrophages. Our results also provide an NK cells‐mediated hepatitis model.