id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-003921-8r8z0otz	Nakamura, Kojiro	The Evolving Role of Neutrophils in Liver Transplant Ischemia-Reperfusion Injury	2019-01-29		.txt	text/plain	6688	318	25	PURPOSE OF REVIEW: Hepatic ischemia-reperfusion injury (IRI), an inevitable event during liver transplantation, represents a major risk factor for the primary graft dysfunction as well as the development of acute and chronic rejection. In IRI-LT pathophysiology, both Kupffer cells (donor-origin) and liver-infiltrating bone marrow-derived macrophages (recipient-origin) play dominant roles in priming innate immune responses [9] [10] [11] , with the majority of studies focusing on macrophage regulation [12, 13] . Indeed, hepatocyte-specific HMGB1 deficient mice showed decreased hepatic necrosis and neutrophil accumulation, whereas the number of their macrophages remained unchanged in acetaminophen-induced liver injury model [28] . In addition, CXCL1 blocking antibody alleviated hepatic infiltration in necrotic cellinduced neutrophil mobilization model [31] , whereas in a carbon tetrachloride (CCl4)-induced acute liver injury, defective CXCL2 expression in TLR2-knockout or S100A9-knockout mice was accompanied by suppressed hepatic neutrophil recruitment [32] . CD4 T cells promote tissue inflammation via CD40 signaling without de novo activation in a murine model of liver ischemia/reperfusion injury	./cache/cord-003921-8r8z0otz.txt	./txt/cord-003921-8r8z0otz.txt