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A TLR2/S100A9/CXCL-2 signaling network is necessary for neutrophil recruitment in acute and chronic liver injury in the mouse
Authors:Anna Moles  Lindsay Murphy  Caroline L. Wilson  Jayashree Bagchi Chakraborty  Christopher Fox  Eek Joong Park  Jelena Mann  Fiona Oakley  Rachel Howarth  John Brain  Steven Masson  Michael Karin  Ekihiro Seki  Derek A. Mann
Affiliation:1 Fibrosis Research Group, Institute of Cellular Medicine, Newcastle University, Newcastle Upon Tyne, UK;2 Division of Gastroenterology, Department of Medicine, University of California, San Diego, School of Medicine, La Jolla, CA, USA;3 Department of Pharmacology and Pathology Laboratory of Gene Regulation and Signal Transduction, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0723, USA
Abstract:
Keywords:APAP ALF, acetaminophen acute liver failure   AHH, acute alcoholic hepatitis   α-SMA, α-smooth muscle actin   ALT, alanine transaminase   ALD, alcoholic liver disease   CCl4, carbon tetrachloride   CCL-2, chemokine (C-C motif) ligand 2   CCL-5, chemokine (C-C motif) ligand 5   CXCL-2, chemokine (C-X-C motif) ligand 2   CXCL-1, chemokine (C-X-C motif) ligand 1   IHC, immunohistochemistry   IL6, interleukin-6   LTA, lipoteichoic acid   NASH, non-alcoholic steatohepatitis   PBC, primary biliary cirrhosis   PSC, primary sclerosing cholangitis   PCNA, proliferating cell nuclear antigen   ROS, reactive oxygen species   S100A8, S100 calcium binding protein A8   S100A9, S100 calcium binding protein A9   TLR, toll like receptor   TNF-α, tumor necrosis factor-α
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