Abstract
Hepatic ischemia and reperfusion elicits an immune response that lacks a microbial constituent yet poses a potentially lethal threat to the host. In this sterile setting, the immune system is alarmed by endogenous danger signals that are release by stressed and dying liver cells. The detection of these immunogenic messengers by sentinel leukocyte populations constitutes the proximal trigger for a self-perpetuating cycle of inflammation, in which consecutive waves of cytokines and chemokines orchestrate the influx of various leukocyte subsets that ultimately confer tissue destruction. This review focuses on the temporal organization of sterile hepatic inflammation, using surgery-induced trauma as a template disease state.
Published Version
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