Antifibrotic Effects of CXCL9 and Its Receptor CXCR3 in Livers of Mice and Humans
Background & Aims Fibrosis is the hallmark of chronic liver diseases, yet many aspects of its mechanism remain to be defined. Chemokines are ubiquitous chemotactic molecules that mediate many acute and chronic inflammatory conditions, and CXC chemokine genes colocalize with a locus previously sh...
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| Veröffentlicht in: | Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 2009-07, Vol.137 (1), p.309-319.e3 |
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| creator | Wasmuth, Hermann E Lammert, Frank Zaldivar, Mirko Moreno Weiskirchen, Ralf Hellerbrand, Claus Scholten, David Berres, Marie-Luise Zimmermann, Henning Streetz, Konrad L Tacke, Frank Hillebrandt, Sonja Schmitz, Petra Keppeler, Hildegard Berg, Thomas Dahl, Edgar Gassler, Nikolaus Friedman, Scott L Trautwein, Christian |
| description | Background & Aims Fibrosis is the hallmark of chronic liver diseases, yet many aspects of its mechanism remain to be defined. Chemokines are ubiquitous chemotactic molecules that mediate many acute and chronic inflammatory conditions, and CXC chemokine genes colocalize with a locus previously shown to include fibrogenic genes. We investigated the roles of the chemokine CXCL9 and its receptor CXCR3 in liver fibrosis. Methods The effects of CXCL variants on fibrogenesis were analyzed using samples from patients with hepatitis C virus infection and by induction of fibrosis in CXCR3−/− and wild-type mice. In mice, intrahepatic immune cell subsets were investigated and interferon gamma messenger RNA levels were measured at baseline and after injury. Human serum CXCL9 levels were measured and correlated with CXCL9 variant and fibrosis severity. The effects of stimulation with CXCL9 were investigated on human hepatic stellate cells (LX-2). Results Specific CXCL9 variants were associated with liver fibrosis in mice and humans; CXCL9 serum concentrations correlated with genotypes and levels of fibrosis in patients. In contrast to other chemokines, CXCL9 exerted antifibrotic effects in vitro, suppressing collagen production in LX-2 cells. CXCR3−/− mice had increased liver fibrosis; progression was associated with decreased numbers of intrahepatic interferon gamma–positive T cells and reduced interferon gamma messenger RNA, indicating that CXCL9-CXCR3 regulates Th1-associated immune pathways. Conclusions This is the first description of a chemokine-based antifibrotic pathway in the liver; antifibrotic therapies might be developed to modulate CXC chemokine levels. |
| doi_str_mv | 10.1053/j.gastro.2009.03.053 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2892869</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>1_s2_0_S0016508509005174</els_id><sourcerecordid>19344719</sourcerecordid><originalsourceid>FETCH-LOGICAL-c582t-dac89ce930680c3d75f90eee51f8772e25f997b6f54928db2990be5b26dd84a23</originalsourceid><addsrcrecordid>eNqFkdFuFCEUhonR2LX6BsbMC8x4gGEGbkyaTbVN1hjbmnhHGDhU1t1hA7Ob9O1luo3V3vTqhJ___Ae-Q8h7Cg0FwT-um1uTpxQbBqAa4E0RX5AFFUzWAJS9JItSulqAFCfkTc5rKEYu6WtyQhVv256qBfl-Nk7BhyHFKdjq3Hu0U66ir5Y_lytVmdFVl0W4Qou7KaZZvuJVGKtVOGC6d34NFu-NF_utGfNb8sqbTcZ3D_WU_Ph8frO8qFffvlwuz1a1FZJNtTNWKouKQyfBctcLrwARBfWy7xmyclb90HnRKibdwJSCAcXAOudkaxg_JZ-Oubv9sEVncZyS2ehdCluT7nQ0Qf9_M4Zf-jYeNJMlsFMloD0G2BRzTuj_9lLQM2K91kfEekasgesilrYP_859bHpg-vgwLL8_BEw624CjRRdSoatdDM9NeBpgN2EM1mx-4x3mddynsZDVVGemQV_Pa563DApA0L7lfwCEa6Oh</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Antifibrotic Effects of CXCL9 and Its Receptor CXCR3 in Livers of Mice and Humans</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><source>Alma/SFX Local Collection</source><creator>Wasmuth, Hermann E ; Lammert, Frank ; Zaldivar, Mirko Moreno ; Weiskirchen, Ralf ; Hellerbrand, Claus ; Scholten, David ; Berres, Marie-Luise ; Zimmermann, Henning ; Streetz, Konrad L ; Tacke, Frank ; Hillebrandt, Sonja ; Schmitz, Petra ; Keppeler, Hildegard ; Berg, Thomas ; Dahl, Edgar ; Gassler, Nikolaus ; Friedman, Scott L ; Trautwein, Christian</creator><creatorcontrib>Wasmuth, Hermann E ; Lammert, Frank ; Zaldivar, Mirko Moreno ; Weiskirchen, Ralf ; Hellerbrand, Claus ; Scholten, David ; Berres, Marie-Luise ; Zimmermann, Henning ; Streetz, Konrad L ; Tacke, Frank ; Hillebrandt, Sonja ; Schmitz, Petra ; Keppeler, Hildegard ; Berg, Thomas ; Dahl, Edgar ; Gassler, Nikolaus ; Friedman, Scott L ; Trautwein, Christian</creatorcontrib><description>Background & Aims Fibrosis is the hallmark of chronic liver diseases, yet many aspects of its mechanism remain to be defined. Chemokines are ubiquitous chemotactic molecules that mediate many acute and chronic inflammatory conditions, and CXC chemokine genes colocalize with a locus previously shown to include fibrogenic genes. We investigated the roles of the chemokine CXCL9 and its receptor CXCR3 in liver fibrosis. Methods The effects of CXCL variants on fibrogenesis were analyzed using samples from patients with hepatitis C virus infection and by induction of fibrosis in CXCR3−/− and wild-type mice. In mice, intrahepatic immune cell subsets were investigated and interferon gamma messenger RNA levels were measured at baseline and after injury. Human serum CXCL9 levels were measured and correlated with CXCL9 variant and fibrosis severity. The effects of stimulation with CXCL9 were investigated on human hepatic stellate cells (LX-2). Results Specific CXCL9 variants were associated with liver fibrosis in mice and humans; CXCL9 serum concentrations correlated with genotypes and levels of fibrosis in patients. In contrast to other chemokines, CXCL9 exerted antifibrotic effects in vitro, suppressing collagen production in LX-2 cells. CXCR3−/− mice had increased liver fibrosis; progression was associated with decreased numbers of intrahepatic interferon gamma–positive T cells and reduced interferon gamma messenger RNA, indicating that CXCL9-CXCR3 regulates Th1-associated immune pathways. Conclusions This is the first description of a chemokine-based antifibrotic pathway in the liver; antifibrotic therapies might be developed to modulate CXC chemokine levels.</description><identifier>ISSN: 0016-5085</identifier><identifier>EISSN: 1528-0012</identifier><identifier>DOI: 10.1053/j.gastro.2009.03.053</identifier><identifier>PMID: 19344719</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Carbon Tetrachloride ; Cells, Cultured ; Chemokine CXCL9 - blood ; Chemokine CXCL9 - genetics ; Chemokine CXCL9 - metabolism ; Cohort Studies ; Collagen - metabolism ; Disease Models, Animal ; Gastroenterology and Hepatology ; Genotype ; Hepatic Stellate Cells - immunology ; Hepatitis C, Chronic - complications ; Hepatitis C, Chronic - immunology ; Humans ; Interferon-gamma - metabolism ; Liver - immunology ; Liver - metabolism ; Liver - pathology ; Liver - virology ; Liver Cirrhosis - chemically induced ; Liver Cirrhosis - immunology ; Liver Cirrhosis - pathology ; Liver Cirrhosis - prevention & control ; Liver Cirrhosis - virology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Phenotype ; Polymorphism, Single Nucleotide ; Receptors, CXCR3 - deficiency ; Receptors, CXCR3 - genetics ; Receptors, CXCR3 - metabolism ; RNA, Messenger - metabolism ; Severity of Illness Index ; Th1 Cells - immunology</subject><ispartof>Gastroenterology (New York, N.Y. 1943), 2009-07, Vol.137 (1), p.309-319.e3</ispartof><rights>AGA Institute</rights><rights>2009 AGA Institute</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c582t-dac89ce930680c3d75f90eee51f8772e25f997b6f54928db2990be5b26dd84a23</citedby><cites>FETCH-LOGICAL-c582t-dac89ce930680c3d75f90eee51f8772e25f997b6f54928db2990be5b26dd84a23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1053/j.gastro.2009.03.053$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19344719$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wasmuth, Hermann E</creatorcontrib><creatorcontrib>Lammert, Frank</creatorcontrib><creatorcontrib>Zaldivar, Mirko Moreno</creatorcontrib><creatorcontrib>Weiskirchen, Ralf</creatorcontrib><creatorcontrib>Hellerbrand, Claus</creatorcontrib><creatorcontrib>Scholten, David</creatorcontrib><creatorcontrib>Berres, Marie-Luise</creatorcontrib><creatorcontrib>Zimmermann, Henning</creatorcontrib><creatorcontrib>Streetz, Konrad L</creatorcontrib><creatorcontrib>Tacke, Frank</creatorcontrib><creatorcontrib>Hillebrandt, Sonja</creatorcontrib><creatorcontrib>Schmitz, Petra</creatorcontrib><creatorcontrib>Keppeler, Hildegard</creatorcontrib><creatorcontrib>Berg, Thomas</creatorcontrib><creatorcontrib>Dahl, Edgar</creatorcontrib><creatorcontrib>Gassler, Nikolaus</creatorcontrib><creatorcontrib>Friedman, Scott L</creatorcontrib><creatorcontrib>Trautwein, Christian</creatorcontrib><title>Antifibrotic Effects of CXCL9 and Its Receptor CXCR3 in Livers of Mice and Humans</title><title>Gastroenterology (New York, N.Y. 1943)</title><addtitle>Gastroenterology</addtitle><description>Background & Aims Fibrosis is the hallmark of chronic liver diseases, yet many aspects of its mechanism remain to be defined. Chemokines are ubiquitous chemotactic molecules that mediate many acute and chronic inflammatory conditions, and CXC chemokine genes colocalize with a locus previously shown to include fibrogenic genes. We investigated the roles of the chemokine CXCL9 and its receptor CXCR3 in liver fibrosis. Methods The effects of CXCL variants on fibrogenesis were analyzed using samples from patients with hepatitis C virus infection and by induction of fibrosis in CXCR3−/− and wild-type mice. In mice, intrahepatic immune cell subsets were investigated and interferon gamma messenger RNA levels were measured at baseline and after injury. Human serum CXCL9 levels were measured and correlated with CXCL9 variant and fibrosis severity. The effects of stimulation with CXCL9 were investigated on human hepatic stellate cells (LX-2). Results Specific CXCL9 variants were associated with liver fibrosis in mice and humans; CXCL9 serum concentrations correlated with genotypes and levels of fibrosis in patients. In contrast to other chemokines, CXCL9 exerted antifibrotic effects in vitro, suppressing collagen production in LX-2 cells. CXCR3−/− mice had increased liver fibrosis; progression was associated with decreased numbers of intrahepatic interferon gamma–positive T cells and reduced interferon gamma messenger RNA, indicating that CXCL9-CXCR3 regulates Th1-associated immune pathways. Conclusions This is the first description of a chemokine-based antifibrotic pathway in the liver; antifibrotic therapies might be developed to modulate CXC chemokine levels.</description><subject>Animals</subject><subject>Carbon Tetrachloride</subject><subject>Cells, Cultured</subject><subject>Chemokine CXCL9 - blood</subject><subject>Chemokine CXCL9 - genetics</subject><subject>Chemokine CXCL9 - metabolism</subject><subject>Cohort Studies</subject><subject>Collagen - metabolism</subject><subject>Disease Models, Animal</subject><subject>Gastroenterology and Hepatology</subject><subject>Genotype</subject><subject>Hepatic Stellate Cells - immunology</subject><subject>Hepatitis C, Chronic - complications</subject><subject>Hepatitis C, Chronic - immunology</subject><subject>Humans</subject><subject>Interferon-gamma - metabolism</subject><subject>Liver - immunology</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver - virology</subject><subject>Liver Cirrhosis - chemically induced</subject><subject>Liver Cirrhosis - immunology</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver Cirrhosis - prevention & control</subject><subject>Liver Cirrhosis - virology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Phenotype</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Receptors, CXCR3 - deficiency</subject><subject>Receptors, CXCR3 - genetics</subject><subject>Receptors, CXCR3 - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Severity of Illness Index</subject><subject>Th1 Cells - immunology</subject><issn>0016-5085</issn><issn>1528-0012</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkdFuFCEUhonR2LX6BsbMC8x4gGEGbkyaTbVN1hjbmnhHGDhU1t1hA7Ob9O1luo3V3vTqhJ___Ae-Q8h7Cg0FwT-um1uTpxQbBqAa4E0RX5AFFUzWAJS9JItSulqAFCfkTc5rKEYu6WtyQhVv256qBfl-Nk7BhyHFKdjq3Hu0U66ir5Y_lytVmdFVl0W4Qou7KaZZvuJVGKtVOGC6d34NFu-NF_utGfNb8sqbTcZ3D_WU_Ph8frO8qFffvlwuz1a1FZJNtTNWKouKQyfBctcLrwARBfWy7xmyclb90HnRKibdwJSCAcXAOudkaxg_JZ-Oubv9sEVncZyS2ehdCluT7nQ0Qf9_M4Zf-jYeNJMlsFMloD0G2BRzTuj_9lLQM2K91kfEekasgesilrYP_859bHpg-vgwLL8_BEw624CjRRdSoatdDM9NeBpgN2EM1mx-4x3mddynsZDVVGemQV_Pa563DApA0L7lfwCEa6Oh</recordid><startdate>20090701</startdate><enddate>20090701</enddate><creator>Wasmuth, Hermann E</creator><creator>Lammert, Frank</creator><creator>Zaldivar, Mirko Moreno</creator><creator>Weiskirchen, Ralf</creator><creator>Hellerbrand, Claus</creator><creator>Scholten, David</creator><creator>Berres, Marie-Luise</creator><creator>Zimmermann, Henning</creator><creator>Streetz, Konrad L</creator><creator>Tacke, Frank</creator><creator>Hillebrandt, Sonja</creator><creator>Schmitz, Petra</creator><creator>Keppeler, Hildegard</creator><creator>Berg, Thomas</creator><creator>Dahl, Edgar</creator><creator>Gassler, Nikolaus</creator><creator>Friedman, Scott L</creator><creator>Trautwein, Christian</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20090701</creationdate><title>Antifibrotic Effects of CXCL9 and Its Receptor CXCR3 in Livers of Mice and Humans</title><author>Wasmuth, Hermann E ; Lammert, Frank ; Zaldivar, Mirko Moreno ; Weiskirchen, Ralf ; Hellerbrand, Claus ; Scholten, David ; Berres, Marie-Luise ; Zimmermann, Henning ; Streetz, Konrad L ; Tacke, Frank ; Hillebrandt, Sonja ; Schmitz, Petra ; Keppeler, Hildegard ; Berg, Thomas ; Dahl, Edgar ; Gassler, Nikolaus ; Friedman, Scott L ; Trautwein, Christian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c582t-dac89ce930680c3d75f90eee51f8772e25f997b6f54928db2990be5b26dd84a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Carbon Tetrachloride</topic><topic>Cells, Cultured</topic><topic>Chemokine CXCL9 - blood</topic><topic>Chemokine CXCL9 - genetics</topic><topic>Chemokine CXCL9 - metabolism</topic><topic>Cohort Studies</topic><topic>Collagen - metabolism</topic><topic>Disease Models, Animal</topic><topic>Gastroenterology and Hepatology</topic><topic>Genotype</topic><topic>Hepatic Stellate Cells - immunology</topic><topic>Hepatitis C, Chronic - complications</topic><topic>Hepatitis C, Chronic - immunology</topic><topic>Humans</topic><topic>Interferon-gamma - metabolism</topic><topic>Liver - immunology</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver - virology</topic><topic>Liver Cirrhosis - chemically induced</topic><topic>Liver Cirrhosis - immunology</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver Cirrhosis - prevention & control</topic><topic>Liver Cirrhosis - virology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Phenotype</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Receptors, CXCR3 - deficiency</topic><topic>Receptors, CXCR3 - genetics</topic><topic>Receptors, CXCR3 - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Severity of Illness Index</topic><topic>Th1 Cells - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wasmuth, Hermann E</creatorcontrib><creatorcontrib>Lammert, Frank</creatorcontrib><creatorcontrib>Zaldivar, Mirko Moreno</creatorcontrib><creatorcontrib>Weiskirchen, Ralf</creatorcontrib><creatorcontrib>Hellerbrand, Claus</creatorcontrib><creatorcontrib>Scholten, David</creatorcontrib><creatorcontrib>Berres, Marie-Luise</creatorcontrib><creatorcontrib>Zimmermann, Henning</creatorcontrib><creatorcontrib>Streetz, Konrad L</creatorcontrib><creatorcontrib>Tacke, Frank</creatorcontrib><creatorcontrib>Hillebrandt, Sonja</creatorcontrib><creatorcontrib>Schmitz, Petra</creatorcontrib><creatorcontrib>Keppeler, Hildegard</creatorcontrib><creatorcontrib>Berg, Thomas</creatorcontrib><creatorcontrib>Dahl, Edgar</creatorcontrib><creatorcontrib>Gassler, Nikolaus</creatorcontrib><creatorcontrib>Friedman, Scott L</creatorcontrib><creatorcontrib>Trautwein, Christian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wasmuth, Hermann E</au><au>Lammert, Frank</au><au>Zaldivar, Mirko Moreno</au><au>Weiskirchen, Ralf</au><au>Hellerbrand, Claus</au><au>Scholten, David</au><au>Berres, Marie-Luise</au><au>Zimmermann, Henning</au><au>Streetz, Konrad L</au><au>Tacke, Frank</au><au>Hillebrandt, Sonja</au><au>Schmitz, Petra</au><au>Keppeler, Hildegard</au><au>Berg, Thomas</au><au>Dahl, Edgar</au><au>Gassler, Nikolaus</au><au>Friedman, Scott L</au><au>Trautwein, Christian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antifibrotic Effects of CXCL9 and Its Receptor CXCR3 in Livers of Mice and Humans</atitle><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle><addtitle>Gastroenterology</addtitle><date>2009-07-01</date><risdate>2009</risdate><volume>137</volume><issue>1</issue><spage>309</spage><epage>319.e3</epage><pages>309-319.e3</pages><issn>0016-5085</issn><eissn>1528-0012</eissn><abstract>Background & Aims Fibrosis is the hallmark of chronic liver diseases, yet many aspects of its mechanism remain to be defined. Chemokines are ubiquitous chemotactic molecules that mediate many acute and chronic inflammatory conditions, and CXC chemokine genes colocalize with a locus previously shown to include fibrogenic genes. We investigated the roles of the chemokine CXCL9 and its receptor CXCR3 in liver fibrosis. Methods The effects of CXCL variants on fibrogenesis were analyzed using samples from patients with hepatitis C virus infection and by induction of fibrosis in CXCR3−/− and wild-type mice. In mice, intrahepatic immune cell subsets were investigated and interferon gamma messenger RNA levels were measured at baseline and after injury. Human serum CXCL9 levels were measured and correlated with CXCL9 variant and fibrosis severity. The effects of stimulation with CXCL9 were investigated on human hepatic stellate cells (LX-2). Results Specific CXCL9 variants were associated with liver fibrosis in mice and humans; CXCL9 serum concentrations correlated with genotypes and levels of fibrosis in patients. In contrast to other chemokines, CXCL9 exerted antifibrotic effects in vitro, suppressing collagen production in LX-2 cells. CXCR3−/− mice had increased liver fibrosis; progression was associated with decreased numbers of intrahepatic interferon gamma–positive T cells and reduced interferon gamma messenger RNA, indicating that CXCL9-CXCR3 regulates Th1-associated immune pathways. Conclusions This is the first description of a chemokine-based antifibrotic pathway in the liver; antifibrotic therapies might be developed to modulate CXC chemokine levels.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>19344719</pmid><doi>10.1053/j.gastro.2009.03.053</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Carbon Tetrachloride Cells, Cultured Chemokine CXCL9 - blood Chemokine CXCL9 - genetics Chemokine CXCL9 - metabolism Cohort Studies Collagen - metabolism Disease Models, Animal Gastroenterology and Hepatology Genotype Hepatic Stellate Cells - immunology Hepatitis C, Chronic - complications Hepatitis C, Chronic - immunology Humans Interferon-gamma - metabolism Liver - immunology Liver - metabolism Liver - pathology Liver - virology Liver Cirrhosis - chemically induced Liver Cirrhosis - immunology Liver Cirrhosis - pathology Liver Cirrhosis - prevention & control Liver Cirrhosis - virology Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Phenotype Polymorphism, Single Nucleotide Receptors, CXCR3 - deficiency Receptors, CXCR3 - genetics Receptors, CXCR3 - metabolism RNA, Messenger - metabolism Severity of Illness Index Th1 Cells - immunology |
| title | Antifibrotic Effects of CXCL9 and Its Receptor CXCR3 in Livers of Mice and Humans |
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