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http://purl.uniprot.org/citations/10570316http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10570316http://www.w3.org/2000/01/rdf-schema#comment"The role played by chemokines in regulating the selective recruitment of lymphocytes to different tissue compartments in disease is poorly characterized. In hepatitis C infection, inflammation confined to portal areas is associated with a less aggressive course, whereas T cell infiltration of the liver parenchyma is associated with progressive liver injury and cirrhosis. We propose a mechanism to explain how lymphocytes are recruited to hepatic lobules during bursts of necroinflammatory activity in chronic hepatitis C infection. We report here that lymphocytes infiltrating hepatitis C-infected liver express high levels of the chemokine receptors CCR5 and CXCR3. However, whereas the CCR5 ligands macrophage inflammatory protein-1alpha and -1beta were largely confined to vessels within portal tracts, the CXCR3 ligands IFN-inducible protein-10 and monokine-induced by IFN-gamma were selectively up-regulated on sinusoidal endothelium. In vitro, human hepatic sinusoidal endothelial cells secreted IFN-inducible protein-10 and monokine-induced by IFN-gamma in response to stimulation with IFN-gamma in combination with either IL-1 or TNF-alpha. This suggests that intrahepatic Th1 cytokines drive the increased expression of IFN-inducible protein-10 and monokine-induced by IFN-gamma and thereby promote the continuing recruitment of CXCR3-expressing T cells into the hepatic lobule in chronic hepatitis C infection."xsd:string
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/author"Qin S."xsd:string
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/author"Adams D.H."xsd:string
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/author"Salmon M."xsd:string
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/author"Hubscher S.G."xsd:string
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/author"Morland C.M."xsd:string
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/author"Shields P.L."xsd:string
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/date"1999"xsd:gYear
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/pages"6236-6243"xsd:string
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/title"Chemokine and chemokine receptor interactions provide a mechanism for selective T cell recruitment to specific liver compartments within hepatitis C-infected liver."xsd:string
http://purl.uniprot.org/citations/10570316http://purl.uniprot.org/core/volume"163"xsd:string
http://purl.uniprot.org/citations/10570316http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/10570316
http://purl.uniprot.org/citations/10570316http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/10570316
http://purl.uniprot.org/uniprot/Q07325#attribution-10EAA6DDCB0CA037A6A3A2FF9A22C16Ahttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/10570316