Interleukin-1 and inflammasomes in XXXX and @entity1561 / @entity1561 .

@entity1 @entity32 @entity82 @entity5881 @entity99 @entity1560 @entity39 @entity5 @entity19 @entity221 @entity409 @entity5003 @entity1561 @entity209 @entity157 @entity1990 @entity1068 @entity4795
UNASSIGNED: Both @entity5881 ( @entity5881 ) and @entity1561 are characterized by massive lipid accumulation in the liver accompanied by @entity32 , @entity82 , @entity82 , and @entity157 in a substantial subgroup of @entity1 . At several stages in these diseases, mediators of the immune system, such as cytokines or inflammasomes, are crucially involved. In @entity5881 , chronic @entity1068 exposure sensitizes Kupffer cells to activation by lipopolysaccharides through Toll-like receptors, e.g., @entity1990 . This sensitization enhances the production of various proinflammatory cytokines such as interleukin-1 ( @entity5003 ) and @entity5 @entity39 factor-alpha, thereby contributing to @entity409 , @entity39 , and apoptosis and the generation of extracellular matrix proteins leading to @entity82 / @entity82 . Indeed, neutralization of @entity5003 by @entity5003 receptor antagonist has recently been shown to potently prevent @entity99 in @entity19 models of @entity5881 . As @entity5003 is clearly linked to key clinical symptoms of @entity99 such as @entity221 , @entity4795 , and wasting, interfering with the @entity5003 pathway might be an attractive treatment strategy in the future. An important role for @entity5003 -type cytokines and certain inflammasomes has also been demonstrated in @entity19 models of @entity1561 . @entity5003 -type cytokines can regulate @entity1560 ; the NLR family pyrin domain containing 3 inflammasome is critically involved in @entity209 . CONCLUSION: @entity5003 cytokine family members and various inflammasomes mediate different aspects of both @entity5881 and @entity1561 . (Hepatology 2016;64:955-965).
