Protein S exacerbates alcoholic hepatitis by stimulating liver natural killer T cells
Summary Background Alcohol consumption is a major cause of liver injury but the mechanisms are not completely understood. Protein S (PS) is an anticoagulant glycoprotein with multiple functions. The role of PS in liver injury is unknown. Objectives This study investigated the role of PS in acute alc...
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| Veröffentlicht in: | Journal of thrombosis and haemostasis 2015-01, Vol.13 (1), p.142-154 |
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| creator | Chelakkot‐Govindalayathil, A.‐L. Mifuji‐Moroka, R. D'Alessandro‐Gabazza, C. N. Toda, M. Matsuda, Y. Gil‐Bernabe, P. Roeen, Z. Yasuma, T. Yano, Y. Gabazza, E. C. Iwasa, M. Takei, Y. |
| description | Summary
Background
Alcohol consumption is a major cause of liver injury but the mechanisms are not completely understood. Protein S (PS) is an anticoagulant glycoprotein with multiple functions. The role of PS in liver injury is unknown.
Objectives
This study investigated the role of PS in acute alcoholic hepatitis.
Methods
A mouse overexpressing human PS (hPS‐TG) was generated in which acute hepatitis was induced by intraperitoneal injection of ethanol.
Results
The levels of serum liver enzymes and liver tissue inflammatory cytokines and the degree of hepatic steatosis were significantly increased in hPS‐TG mice treated with ethanol compared with ethanol‐treated wild type (WT) mice. Cell expansion, activation and inhibition of apoptosis were significantly augmented in natural killer T (NKT) cells from hPS‐TG mice compared with WT mice. Liver mononuclear cells from hPS‐TG mice express higher levels of inflammatory cytokines than those from WT mice after stimulation with a specific stimulant of NKT cells in vitro. In a co‐culture system of hepatocytes and NKT cells, the effects of PS on ethanol‐mediated cell injury were suppressed by a CD1d neutralizing antibody. Alcoholic liver injury was significantly improved in mice pre‐treated with PS siRNA and anti‐protein S antibody compared with control mice. Patients with alcoholic hepatitis showed significantly increased plasma PS levels and enhanced liver expression of PS and CD1d compared with controls.
Conclusions
The results of this study suggest that PS exacerbates acute alcoholic hepatitis by inhibiting apoptosis of activated NKT cells. |
| doi_str_mv | 10.1111/jth.12789 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1644721472</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3555742951</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5079-b416ad4f09405e222f71c0015d547b6188034e7488a5a66c95555b12d8279eaa3</originalsourceid><addsrcrecordid>eNp1kEFLAzEQhYMotlYP_gEJePKwbZJNNpujFLVKQcH2HLK7WZua7tYkq_bfG13rzYFh5sHHm-EBcI7RGMearMNqjAnPxQEYYpbmCc_T7HC_izQdgBPv1whhwQg6BgPCUiEYpkOwfHJt0KaBz1B_qlK7QgXtobJlu2qtKeFKb1UwwXhY7KAPZtPZqJsXaM27drBRoXPKwldjbZQLWGpr_Sk4qpX1-ux3jsDy9mYxnSXzx7v76fU8KRniIikozlRFayQoYpoQUnNcxi9ZxSgvMpznKKWa0zxXTGVZKVisApMqJ1xopdIRuOx9t65967QPct12roknJc4o5QTHjtRVT5Wu9d7pWm6d2Si3kxjJ7wBlDFD-BBjZi1_Hrtjo6o_cJxaBSQ98GKt3_zvJh8Wst_wCPYV5MQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1644721472</pqid></control><display><type>article</type><title>Protein S exacerbates alcoholic hepatitis by stimulating liver natural killer T cells</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Chelakkot‐Govindalayathil, A.‐L. ; Mifuji‐Moroka, R. ; D'Alessandro‐Gabazza, C. N. ; Toda, M. ; Matsuda, Y. ; Gil‐Bernabe, P. ; Roeen, Z. ; Yasuma, T. ; Yano, Y. ; Gabazza, E. C. ; Iwasa, M. ; Takei, Y.</creator><creatorcontrib>Chelakkot‐Govindalayathil, A.‐L. ; Mifuji‐Moroka, R. ; D'Alessandro‐Gabazza, C. N. ; Toda, M. ; Matsuda, Y. ; Gil‐Bernabe, P. ; Roeen, Z. ; Yasuma, T. ; Yano, Y. ; Gabazza, E. C. ; Iwasa, M. ; Takei, Y.</creatorcontrib><description>Summary
Background
Alcohol consumption is a major cause of liver injury but the mechanisms are not completely understood. Protein S (PS) is an anticoagulant glycoprotein with multiple functions. The role of PS in liver injury is unknown.
Objectives
This study investigated the role of PS in acute alcoholic hepatitis.
Methods
A mouse overexpressing human PS (hPS‐TG) was generated in which acute hepatitis was induced by intraperitoneal injection of ethanol.
Results
The levels of serum liver enzymes and liver tissue inflammatory cytokines and the degree of hepatic steatosis were significantly increased in hPS‐TG mice treated with ethanol compared with ethanol‐treated wild type (WT) mice. Cell expansion, activation and inhibition of apoptosis were significantly augmented in natural killer T (NKT) cells from hPS‐TG mice compared with WT mice. Liver mononuclear cells from hPS‐TG mice express higher levels of inflammatory cytokines than those from WT mice after stimulation with a specific stimulant of NKT cells in vitro. In a co‐culture system of hepatocytes and NKT cells, the effects of PS on ethanol‐mediated cell injury were suppressed by a CD1d neutralizing antibody. Alcoholic liver injury was significantly improved in mice pre‐treated with PS siRNA and anti‐protein S antibody compared with control mice. Patients with alcoholic hepatitis showed significantly increased plasma PS levels and enhanced liver expression of PS and CD1d compared with controls.
Conclusions
The results of this study suggest that PS exacerbates acute alcoholic hepatitis by inhibiting apoptosis of activated NKT cells.</description><identifier>ISSN: 1538-7933</identifier><identifier>ISSN: 1538-7836</identifier><identifier>EISSN: 1538-7836</identifier><identifier>DOI: 10.1111/jth.12789</identifier><identifier>PMID: 25399514</identifier><language>eng</language><publisher>England: Elsevier Limited</publisher><subject>alcoholism ; Animals ; Antibodies, Neutralizing - pharmacology ; anticoagulants ; Antigens, CD1d - immunology ; Antigens, CD1d - metabolism ; Apoptosis ; Blood Proteins - genetics ; Blood Proteins - metabolism ; Case-Control Studies ; Cells, Cultured ; Coculture Techniques ; Cytokines ; Disease Models, Animal ; Ethanol ; Fatty Liver, Alcoholic - immunology ; Fatty Liver, Alcoholic - metabolism ; Fatty Liver, Alcoholic - pathology ; hepatitis ; Hepatitis, Alcoholic - genetics ; Hepatitis, Alcoholic - immunology ; Hepatitis, Alcoholic - metabolism ; Hepatitis, Alcoholic - pathology ; Hepatitis, Alcoholic - prevention & control ; Hepatocytes - immunology ; Hepatocytes - metabolism ; Hepatocytes - pathology ; Humans ; Inflammation Mediators - immunology ; Inflammation Mediators - metabolism ; Liver - immunology ; Liver - metabolism ; Liver - pathology ; Liver cirrhosis ; Lymphocyte Activation ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; natural killer T cells ; Natural Killer T-Cells - immunology ; Natural Killer T-Cells - metabolism ; protein S ; Protein S - genetics ; Protein S - metabolism ; Proteins ; RNAi Therapeutics ; Rodents ; Severity of Illness Index ; Signal Transduction ; T cell receptors ; Up-Regulation</subject><ispartof>Journal of thrombosis and haemostasis, 2015-01, Vol.13 (1), p.142-154</ispartof><rights>2014 International Society on Thrombosis and Haemostasis</rights><rights>2014 International Society on Thrombosis and Haemostasis.</rights><rights>Copyright © 2015 International Society on Thrombosis and Haemostasis</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5079-b416ad4f09405e222f71c0015d547b6188034e7488a5a66c95555b12d8279eaa3</citedby><cites>FETCH-LOGICAL-c5079-b416ad4f09405e222f71c0015d547b6188034e7488a5a66c95555b12d8279eaa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25399514$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chelakkot‐Govindalayathil, A.‐L.</creatorcontrib><creatorcontrib>Mifuji‐Moroka, R.</creatorcontrib><creatorcontrib>D'Alessandro‐Gabazza, C. N.</creatorcontrib><creatorcontrib>Toda, M.</creatorcontrib><creatorcontrib>Matsuda, Y.</creatorcontrib><creatorcontrib>Gil‐Bernabe, P.</creatorcontrib><creatorcontrib>Roeen, Z.</creatorcontrib><creatorcontrib>Yasuma, T.</creatorcontrib><creatorcontrib>Yano, Y.</creatorcontrib><creatorcontrib>Gabazza, E. C.</creatorcontrib><creatorcontrib>Iwasa, M.</creatorcontrib><creatorcontrib>Takei, Y.</creatorcontrib><title>Protein S exacerbates alcoholic hepatitis by stimulating liver natural killer T cells</title><title>Journal of thrombosis and haemostasis</title><addtitle>J Thromb Haemost</addtitle><description>Summary
Background
Alcohol consumption is a major cause of liver injury but the mechanisms are not completely understood. Protein S (PS) is an anticoagulant glycoprotein with multiple functions. The role of PS in liver injury is unknown.
Objectives
This study investigated the role of PS in acute alcoholic hepatitis.
Methods
A mouse overexpressing human PS (hPS‐TG) was generated in which acute hepatitis was induced by intraperitoneal injection of ethanol.
Results
The levels of serum liver enzymes and liver tissue inflammatory cytokines and the degree of hepatic steatosis were significantly increased in hPS‐TG mice treated with ethanol compared with ethanol‐treated wild type (WT) mice. Cell expansion, activation and inhibition of apoptosis were significantly augmented in natural killer T (NKT) cells from hPS‐TG mice compared with WT mice. Liver mononuclear cells from hPS‐TG mice express higher levels of inflammatory cytokines than those from WT mice after stimulation with a specific stimulant of NKT cells in vitro. In a co‐culture system of hepatocytes and NKT cells, the effects of PS on ethanol‐mediated cell injury were suppressed by a CD1d neutralizing antibody. Alcoholic liver injury was significantly improved in mice pre‐treated with PS siRNA and anti‐protein S antibody compared with control mice. Patients with alcoholic hepatitis showed significantly increased plasma PS levels and enhanced liver expression of PS and CD1d compared with controls.
Conclusions
The results of this study suggest that PS exacerbates acute alcoholic hepatitis by inhibiting apoptosis of activated NKT cells.</description><subject>alcoholism</subject><subject>Animals</subject><subject>Antibodies, Neutralizing - pharmacology</subject><subject>anticoagulants</subject><subject>Antigens, CD1d - immunology</subject><subject>Antigens, CD1d - metabolism</subject><subject>Apoptosis</subject><subject>Blood Proteins - genetics</subject><subject>Blood Proteins - metabolism</subject><subject>Case-Control Studies</subject><subject>Cells, Cultured</subject><subject>Coculture Techniques</subject><subject>Cytokines</subject><subject>Disease Models, Animal</subject><subject>Ethanol</subject><subject>Fatty Liver, Alcoholic - immunology</subject><subject>Fatty Liver, Alcoholic - metabolism</subject><subject>Fatty Liver, Alcoholic - pathology</subject><subject>hepatitis</subject><subject>Hepatitis, Alcoholic - genetics</subject><subject>Hepatitis, Alcoholic - immunology</subject><subject>Hepatitis, Alcoholic - metabolism</subject><subject>Hepatitis, Alcoholic - pathology</subject><subject>Hepatitis, Alcoholic - prevention & control</subject><subject>Hepatocytes - immunology</subject><subject>Hepatocytes - metabolism</subject><subject>Hepatocytes - pathology</subject><subject>Humans</subject><subject>Inflammation Mediators - immunology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Liver - immunology</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver cirrhosis</subject><subject>Lymphocyte Activation</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>natural killer T cells</subject><subject>Natural Killer T-Cells - immunology</subject><subject>Natural Killer T-Cells - metabolism</subject><subject>protein S</subject><subject>Protein S - genetics</subject><subject>Protein S - metabolism</subject><subject>Proteins</subject><subject>RNAi Therapeutics</subject><subject>Rodents</subject><subject>Severity of Illness Index</subject><subject>Signal Transduction</subject><subject>T cell receptors</subject><subject>Up-Regulation</subject><issn>1538-7933</issn><issn>1538-7836</issn><issn>1538-7836</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFLAzEQhYMotlYP_gEJePKwbZJNNpujFLVKQcH2HLK7WZua7tYkq_bfG13rzYFh5sHHm-EBcI7RGMearMNqjAnPxQEYYpbmCc_T7HC_izQdgBPv1whhwQg6BgPCUiEYpkOwfHJt0KaBz1B_qlK7QgXtobJlu2qtKeFKb1UwwXhY7KAPZtPZqJsXaM27drBRoXPKwldjbZQLWGpr_Sk4qpX1-ux3jsDy9mYxnSXzx7v76fU8KRniIikozlRFayQoYpoQUnNcxi9ZxSgvMpznKKWa0zxXTGVZKVisApMqJ1xopdIRuOx9t65967QPct12roknJc4o5QTHjtRVT5Wu9d7pWm6d2Si3kxjJ7wBlDFD-BBjZi1_Hrtjo6o_cJxaBSQ98GKt3_zvJh8Wst_wCPYV5MQ</recordid><startdate>201501</startdate><enddate>201501</enddate><creator>Chelakkot‐Govindalayathil, A.‐L.</creator><creator>Mifuji‐Moroka, R.</creator><creator>D'Alessandro‐Gabazza, C. N.</creator><creator>Toda, M.</creator><creator>Matsuda, Y.</creator><creator>Gil‐Bernabe, P.</creator><creator>Roeen, Z.</creator><creator>Yasuma, T.</creator><creator>Yano, Y.</creator><creator>Gabazza, E. C.</creator><creator>Iwasa, M.</creator><creator>Takei, Y.</creator><general>Elsevier Limited</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>7T5</scope><scope>H94</scope><scope>K9.</scope></search><sort><creationdate>201501</creationdate><title>Protein S exacerbates alcoholic hepatitis by stimulating liver natural killer T cells</title><author>Chelakkot‐Govindalayathil, A.‐L. ; Mifuji‐Moroka, R. ; D'Alessandro‐Gabazza, C. N. ; Toda, M. ; Matsuda, Y. ; Gil‐Bernabe, P. ; Roeen, Z. ; Yasuma, T. ; Yano, Y. ; Gabazza, E. C. ; Iwasa, M. ; Takei, Y.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5079-b416ad4f09405e222f71c0015d547b6188034e7488a5a66c95555b12d8279eaa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>alcoholism</topic><topic>Animals</topic><topic>Antibodies, Neutralizing - pharmacology</topic><topic>anticoagulants</topic><topic>Antigens, CD1d - immunology</topic><topic>Antigens, CD1d - metabolism</topic><topic>Apoptosis</topic><topic>Blood Proteins - genetics</topic><topic>Blood Proteins - metabolism</topic><topic>Case-Control Studies</topic><topic>Cells, Cultured</topic><topic>Coculture Techniques</topic><topic>Cytokines</topic><topic>Disease Models, Animal</topic><topic>Ethanol</topic><topic>Fatty Liver, Alcoholic - immunology</topic><topic>Fatty Liver, Alcoholic - metabolism</topic><topic>Fatty Liver, Alcoholic - pathology</topic><topic>hepatitis</topic><topic>Hepatitis, Alcoholic - genetics</topic><topic>Hepatitis, Alcoholic - immunology</topic><topic>Hepatitis, Alcoholic - metabolism</topic><topic>Hepatitis, Alcoholic - pathology</topic><topic>Hepatitis, Alcoholic - prevention & control</topic><topic>Hepatocytes - immunology</topic><topic>Hepatocytes - metabolism</topic><topic>Hepatocytes - pathology</topic><topic>Humans</topic><topic>Inflammation Mediators - immunology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Liver - immunology</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver cirrhosis</topic><topic>Lymphocyte Activation</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>natural killer T cells</topic><topic>Natural Killer T-Cells - immunology</topic><topic>Natural Killer T-Cells - metabolism</topic><topic>protein S</topic><topic>Protein S - genetics</topic><topic>Protein S - metabolism</topic><topic>Proteins</topic><topic>RNAi Therapeutics</topic><topic>Rodents</topic><topic>Severity of Illness Index</topic><topic>Signal Transduction</topic><topic>T cell receptors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chelakkot‐Govindalayathil, A.‐L.</creatorcontrib><creatorcontrib>Mifuji‐Moroka, R.</creatorcontrib><creatorcontrib>D'Alessandro‐Gabazza, C. N.</creatorcontrib><creatorcontrib>Toda, M.</creatorcontrib><creatorcontrib>Matsuda, Y.</creatorcontrib><creatorcontrib>Gil‐Bernabe, P.</creatorcontrib><creatorcontrib>Roeen, Z.</creatorcontrib><creatorcontrib>Yasuma, T.</creatorcontrib><creatorcontrib>Yano, Y.</creatorcontrib><creatorcontrib>Gabazza, E. C.</creatorcontrib><creatorcontrib>Iwasa, M.</creatorcontrib><creatorcontrib>Takei, Y.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Journal of thrombosis and haemostasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chelakkot‐Govindalayathil, A.‐L.</au><au>Mifuji‐Moroka, R.</au><au>D'Alessandro‐Gabazza, C. N.</au><au>Toda, M.</au><au>Matsuda, Y.</au><au>Gil‐Bernabe, P.</au><au>Roeen, Z.</au><au>Yasuma, T.</au><au>Yano, Y.</au><au>Gabazza, E. C.</au><au>Iwasa, M.</au><au>Takei, Y.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protein S exacerbates alcoholic hepatitis by stimulating liver natural killer T cells</atitle><jtitle>Journal of thrombosis and haemostasis</jtitle><addtitle>J Thromb Haemost</addtitle><date>2015-01</date><risdate>2015</risdate><volume>13</volume><issue>1</issue><spage>142</spage><epage>154</epage><pages>142-154</pages><issn>1538-7933</issn><issn>1538-7836</issn><eissn>1538-7836</eissn><abstract>Summary
Background
Alcohol consumption is a major cause of liver injury but the mechanisms are not completely understood. Protein S (PS) is an anticoagulant glycoprotein with multiple functions. The role of PS in liver injury is unknown.
Objectives
This study investigated the role of PS in acute alcoholic hepatitis.
Methods
A mouse overexpressing human PS (hPS‐TG) was generated in which acute hepatitis was induced by intraperitoneal injection of ethanol.
Results
The levels of serum liver enzymes and liver tissue inflammatory cytokines and the degree of hepatic steatosis were significantly increased in hPS‐TG mice treated with ethanol compared with ethanol‐treated wild type (WT) mice. Cell expansion, activation and inhibition of apoptosis were significantly augmented in natural killer T (NKT) cells from hPS‐TG mice compared with WT mice. Liver mononuclear cells from hPS‐TG mice express higher levels of inflammatory cytokines than those from WT mice after stimulation with a specific stimulant of NKT cells in vitro. In a co‐culture system of hepatocytes and NKT cells, the effects of PS on ethanol‐mediated cell injury were suppressed by a CD1d neutralizing antibody. Alcoholic liver injury was significantly improved in mice pre‐treated with PS siRNA and anti‐protein S antibody compared with control mice. Patients with alcoholic hepatitis showed significantly increased plasma PS levels and enhanced liver expression of PS and CD1d compared with controls.
Conclusions
The results of this study suggest that PS exacerbates acute alcoholic hepatitis by inhibiting apoptosis of activated NKT cells.</abstract><cop>England</cop><pub>Elsevier Limited</pub><pmid>25399514</pmid><doi>10.1111/jth.12789</doi><tpages>13</tpages></addata></record> |
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| issn | 1538-7933 1538-7836 1538-7836 |
| language | eng |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | alcoholism Animals Antibodies, Neutralizing - pharmacology anticoagulants Antigens, CD1d - immunology Antigens, CD1d - metabolism Apoptosis Blood Proteins - genetics Blood Proteins - metabolism Case-Control Studies Cells, Cultured Coculture Techniques Cytokines Disease Models, Animal Ethanol Fatty Liver, Alcoholic - immunology Fatty Liver, Alcoholic - metabolism Fatty Liver, Alcoholic - pathology hepatitis Hepatitis, Alcoholic - genetics Hepatitis, Alcoholic - immunology Hepatitis, Alcoholic - metabolism Hepatitis, Alcoholic - pathology Hepatitis, Alcoholic - prevention & control Hepatocytes - immunology Hepatocytes - metabolism Hepatocytes - pathology Humans Inflammation Mediators - immunology Inflammation Mediators - metabolism Liver - immunology Liver - metabolism Liver - pathology Liver cirrhosis Lymphocyte Activation Male Mice, Inbred C57BL Mice, Transgenic natural killer T cells Natural Killer T-Cells - immunology Natural Killer T-Cells - metabolism protein S Protein S - genetics Protein S - metabolism Proteins RNAi Therapeutics Rodents Severity of Illness Index Signal Transduction T cell receptors Up-Regulation |
| title | Protein S exacerbates alcoholic hepatitis by stimulating liver natural killer T cells |
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