Features and distribution of CD8 T cells with human leukocyte antigen class I–specific receptor expression in chronic hepatitis C
CD8+ T cells represent a sizable component of the liver inflammatory infiltrate in chronic hepatitis C and are thought to contribute to immune‐mediated tissue injury. Because chronic stimulation may promote the expression by CD8+ T cells of distinct human leukocyte antigen class I–specific natural k...
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| Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 2007-11, Vol.46 (5), p.1375-1386 |
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| creator | Bonorino, Paula Leroy, Vincent Dufeu‐Duchesne, Tania Tongiani‐Dashan, Stefania Sturm, Nathalie Pernollet, Martine Vivier, Eric Zarski, Jean‐Pierre Marche, Patrice N. Jouvin‐Marche, Evelyne |
| description | CD8+ T cells represent a sizable component of the liver inflammatory infiltrate in chronic hepatitis C and are thought to contribute to immune‐mediated tissue injury. Because chronic stimulation may promote the expression by CD8+ T cells of distinct human leukocyte antigen class I–specific natural killer cell receptors (NKRs) susceptible to both inhibiting effector functions and promoting cell survival, we examined the distribution and characteristics of CD8+ T cells with such receptors in chronic hepatitis C patients. NKR CD8+ T cells were detectable in liver and peripheral blood from hepatitis C virus (HCV)–infected patients but were not major subsets. However, the frequency of NKG2A+ CD8+ in the liver and in a lesser extent in the peripheral blood was positively correlated to histological activity in HCV‐infected patients. No such correlation was found with KIR+ T cells in liver in HCV‐infected patients and with the both NKR CD8+ T cells in hepatitis B virus (HBV) infected patients. Circulating CD8+ T cells expressing KIRs exhibited phenotypic features of memory T cells with exacerbated expression of the senescence marker CD57 in patients. NKG2A+CD8+ T cells were committed T cells that appeared less differentiated than KIR+CD8+ T cells. In HCV‐infected patients, their content in perforin was low and similar to that observed in NKG2A−CD8+ T cells; this scenario was not observed in healthy subjects and HBV‐infected patients. Both NKG2A and KIRs could inhibit the response of HCV‐specific CD8+ T cells ex vivo. Conclusion: These results support the concept that an accumulation in the liver parenchyma of NKR+CD8+ T cells that have functional alterations could be responsible for liver lesions. They provide novel insights into the complexity of liver‐infiltrating CD8+ T cells in chronic hepatitis C and reveal that distinct subsets of antigen‐experienced CD8+ T cells are differentially sensitive to the pervasive influence of HCV (HEPATOLOGY 2007.) |
| doi_str_mv | 10.1002/hep.21850 |
| format | Article |
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Because chronic stimulation may promote the expression by CD8+ T cells of distinct human leukocyte antigen class I–specific natural killer cell receptors (NKRs) susceptible to both inhibiting effector functions and promoting cell survival, we examined the distribution and characteristics of CD8+ T cells with such receptors in chronic hepatitis C patients. NKR CD8+ T cells were detectable in liver and peripheral blood from hepatitis C virus (HCV)–infected patients but were not major subsets. However, the frequency of NKG2A+ CD8+ in the liver and in a lesser extent in the peripheral blood was positively correlated to histological activity in HCV‐infected patients. No such correlation was found with KIR+ T cells in liver in HCV‐infected patients and with the both NKR CD8+ T cells in hepatitis B virus (HBV) infected patients. Circulating CD8+ T cells expressing KIRs exhibited phenotypic features of memory T cells with exacerbated expression of the senescence marker CD57 in patients. NKG2A+CD8+ T cells were committed T cells that appeared less differentiated than KIR+CD8+ T cells. In HCV‐infected patients, their content in perforin was low and similar to that observed in NKG2A−CD8+ T cells; this scenario was not observed in healthy subjects and HBV‐infected patients. Both NKG2A and KIRs could inhibit the response of HCV‐specific CD8+ T cells ex vivo. Conclusion: These results support the concept that an accumulation in the liver parenchyma of NKR+CD8+ T cells that have functional alterations could be responsible for liver lesions. They provide novel insights into the complexity of liver‐infiltrating CD8+ T cells in chronic hepatitis C and reveal that distinct subsets of antigen‐experienced CD8+ T cells are differentially sensitive to the pervasive influence of HCV (HEPATOLOGY 2007.)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.21850</identifier><identifier>PMID: 17668887</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Case-Control Studies ; CD8-Positive T-Lymphocytes - cytology ; CD8-Positive T-Lymphocytes - metabolism ; CD8-Positive T-Lymphocytes - physiology ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Hepatitis B virus ; Hepatitis C virus ; Hepatitis C, Chronic - immunology ; Hepatitis C, Chronic - pathology ; Histocompatibility Antigens Class I - metabolism ; Human viral diseases ; Humans ; Infectious diseases ; Liver - immunology ; Liver - pathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Middle Aged ; NK Cell Lectin-Like Receptor Subfamily C ; Perforin - metabolism ; Phenotype ; Receptors, Immunologic - metabolism ; Receptors, KIR2DL1 - metabolism ; Receptors, KIR2DL3 - metabolism ; Receptors, Natural Killer Cell ; Viral diseases ; Viral hepatitis</subject><ispartof>Hepatology (Baltimore, Md.), 2007-11, Vol.46 (5), p.1375-1386</ispartof><rights>Copyright © 2007 American Association for the Study of Liver Diseases</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4210-6c75345fdc20ee601d344c66fefd7397d2840f18978876f309d695ff3483bb223</citedby><cites>FETCH-LOGICAL-c4210-6c75345fdc20ee601d344c66fefd7397d2840f18978876f309d695ff3483bb223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.21850$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.21850$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19863368$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17668887$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bonorino, Paula</creatorcontrib><creatorcontrib>Leroy, Vincent</creatorcontrib><creatorcontrib>Dufeu‐Duchesne, Tania</creatorcontrib><creatorcontrib>Tongiani‐Dashan, Stefania</creatorcontrib><creatorcontrib>Sturm, Nathalie</creatorcontrib><creatorcontrib>Pernollet, Martine</creatorcontrib><creatorcontrib>Vivier, Eric</creatorcontrib><creatorcontrib>Zarski, Jean‐Pierre</creatorcontrib><creatorcontrib>Marche, Patrice N.</creatorcontrib><creatorcontrib>Jouvin‐Marche, Evelyne</creatorcontrib><title>Features and distribution of CD8 T cells with human leukocyte antigen class I–specific receptor expression in chronic hepatitis C</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>CD8+ T cells represent a sizable component of the liver inflammatory infiltrate in chronic hepatitis C and are thought to contribute to immune‐mediated tissue injury. Because chronic stimulation may promote the expression by CD8+ T cells of distinct human leukocyte antigen class I–specific natural killer cell receptors (NKRs) susceptible to both inhibiting effector functions and promoting cell survival, we examined the distribution and characteristics of CD8+ T cells with such receptors in chronic hepatitis C patients. NKR CD8+ T cells were detectable in liver and peripheral blood from hepatitis C virus (HCV)–infected patients but were not major subsets. However, the frequency of NKG2A+ CD8+ in the liver and in a lesser extent in the peripheral blood was positively correlated to histological activity in HCV‐infected patients. No such correlation was found with KIR+ T cells in liver in HCV‐infected patients and with the both NKR CD8+ T cells in hepatitis B virus (HBV) infected patients. Circulating CD8+ T cells expressing KIRs exhibited phenotypic features of memory T cells with exacerbated expression of the senescence marker CD57 in patients. NKG2A+CD8+ T cells were committed T cells that appeared less differentiated than KIR+CD8+ T cells. In HCV‐infected patients, their content in perforin was low and similar to that observed in NKG2A−CD8+ T cells; this scenario was not observed in healthy subjects and HBV‐infected patients. Both NKG2A and KIRs could inhibit the response of HCV‐specific CD8+ T cells ex vivo. Conclusion: These results support the concept that an accumulation in the liver parenchyma of NKR+CD8+ T cells that have functional alterations could be responsible for liver lesions. They provide novel insights into the complexity of liver‐infiltrating CD8+ T cells in chronic hepatitis C and reveal that distinct subsets of antigen‐experienced CD8+ T cells are differentially sensitive to the pervasive influence of HCV (HEPATOLOGY 2007.)</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>CD8-Positive T-Lymphocytes - cytology</subject><subject>CD8-Positive T-Lymphocytes - metabolism</subject><subject>CD8-Positive T-Lymphocytes - physiology</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hepatitis B virus</subject><subject>Hepatitis C virus</subject><subject>Hepatitis C, Chronic - immunology</subject><subject>Hepatitis C, Chronic - pathology</subject><subject>Histocompatibility Antigens Class I - metabolism</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Liver - immunology</subject><subject>Liver - pathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>NK Cell Lectin-Like Receptor Subfamily C</subject><subject>Perforin - metabolism</subject><subject>Phenotype</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Receptors, KIR2DL1 - metabolism</subject><subject>Receptors, KIR2DL3 - metabolism</subject><subject>Receptors, Natural Killer Cell</subject><subject>Viral diseases</subject><subject>Viral hepatitis</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90c1u1DAUBWALgehQWPACyBsQXaS9_oljL9HQ0kqVyqKsI49zzRgySbAdldkh8Qi8IU-CpzNSV3TlhT-f66NLyGsGpwyAn61xOuVM1_CELFjNm0qIGp6SBfAGKsOEOSIvUvoGAEZy_ZwcsUYprXWzIL8v0OY5YqJ26GgXUo5hNecwDnT0dPlR01vqsO8TvQt5Tdfzxg60x_n76LYZy6McvuJAXW9Told_f_1JE7rgg6MRHU55jBR_TiU_7SJDkes4DuW6_NnmkEOiy5fkmbd9wleH85h8uTi_XV5W1zefrpYfrisnOYNKuaYWsvad44CogHVCSqeUR981wjQd1xI806YpzZQXYDplau-F1GK14lwck3f73CmOP2ZMud2EtCtnBxzn1CotlZHaFPj-UcgaURumoYZCT_bUxTGliL6dYtjYuG0ZtLvltKVoe7-cYt8cYufVBrsHedhGAW8PwCZnex_t4EJ6cEYrIZQu7mzv7kKP2_9PbC_PP-9H_wMLbKcZ</recordid><startdate>200711</startdate><enddate>200711</enddate><creator>Bonorino, Paula</creator><creator>Leroy, Vincent</creator><creator>Dufeu‐Duchesne, Tania</creator><creator>Tongiani‐Dashan, Stefania</creator><creator>Sturm, Nathalie</creator><creator>Pernollet, Martine</creator><creator>Vivier, Eric</creator><creator>Zarski, Jean‐Pierre</creator><creator>Marche, Patrice N.</creator><creator>Jouvin‐Marche, Evelyne</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><scope>IQODW</scope><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>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>200711</creationdate><title>Features and distribution of CD8 T cells with human leukocyte antigen class I–specific receptor expression in chronic hepatitis C</title><author>Bonorino, Paula ; Leroy, Vincent ; Dufeu‐Duchesne, Tania ; Tongiani‐Dashan, Stefania ; Sturm, Nathalie ; Pernollet, Martine ; Vivier, Eric ; Zarski, Jean‐Pierre ; Marche, Patrice N. ; Jouvin‐Marche, Evelyne</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4210-6c75345fdc20ee601d344c66fefd7397d2840f18978876f309d695ff3483bb223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>CD8-Positive T-Lymphocytes - cytology</topic><topic>CD8-Positive T-Lymphocytes - metabolism</topic><topic>CD8-Positive T-Lymphocytes - physiology</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hepatitis B virus</topic><topic>Hepatitis C virus</topic><topic>Hepatitis C, Chronic - immunology</topic><topic>Hepatitis C, Chronic - pathology</topic><topic>Histocompatibility Antigens Class I - metabolism</topic><topic>Human viral diseases</topic><topic>Humans</topic><topic>Infectious diseases</topic><topic>Liver - immunology</topic><topic>Liver - pathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>NK Cell Lectin-Like Receptor Subfamily C</topic><topic>Perforin - metabolism</topic><topic>Phenotype</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Receptors, KIR2DL1 - metabolism</topic><topic>Receptors, KIR2DL3 - metabolism</topic><topic>Receptors, Natural Killer Cell</topic><topic>Viral diseases</topic><topic>Viral hepatitis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bonorino, Paula</creatorcontrib><creatorcontrib>Leroy, Vincent</creatorcontrib><creatorcontrib>Dufeu‐Duchesne, Tania</creatorcontrib><creatorcontrib>Tongiani‐Dashan, Stefania</creatorcontrib><creatorcontrib>Sturm, Nathalie</creatorcontrib><creatorcontrib>Pernollet, Martine</creatorcontrib><creatorcontrib>Vivier, Eric</creatorcontrib><creatorcontrib>Zarski, Jean‐Pierre</creatorcontrib><creatorcontrib>Marche, Patrice N.</creatorcontrib><creatorcontrib>Jouvin‐Marche, Evelyne</creatorcontrib><collection>Pascal-Francis</collection><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>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bonorino, Paula</au><au>Leroy, Vincent</au><au>Dufeu‐Duchesne, Tania</au><au>Tongiani‐Dashan, Stefania</au><au>Sturm, Nathalie</au><au>Pernollet, Martine</au><au>Vivier, Eric</au><au>Zarski, Jean‐Pierre</au><au>Marche, Patrice N.</au><au>Jouvin‐Marche, Evelyne</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Features and distribution of CD8 T cells with human leukocyte antigen class I–specific receptor expression in chronic hepatitis C</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>2007-11</date><risdate>2007</risdate><volume>46</volume><issue>5</issue><spage>1375</spage><epage>1386</epage><pages>1375-1386</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>CD8+ T cells represent a sizable component of the liver inflammatory infiltrate in chronic hepatitis C and are thought to contribute to immune‐mediated tissue injury. Because chronic stimulation may promote the expression by CD8+ T cells of distinct human leukocyte antigen class I–specific natural killer cell receptors (NKRs) susceptible to both inhibiting effector functions and promoting cell survival, we examined the distribution and characteristics of CD8+ T cells with such receptors in chronic hepatitis C patients. NKR CD8+ T cells were detectable in liver and peripheral blood from hepatitis C virus (HCV)–infected patients but were not major subsets. However, the frequency of NKG2A+ CD8+ in the liver and in a lesser extent in the peripheral blood was positively correlated to histological activity in HCV‐infected patients. No such correlation was found with KIR+ T cells in liver in HCV‐infected patients and with the both NKR CD8+ T cells in hepatitis B virus (HBV) infected patients. Circulating CD8+ T cells expressing KIRs exhibited phenotypic features of memory T cells with exacerbated expression of the senescence marker CD57 in patients. NKG2A+CD8+ T cells were committed T cells that appeared less differentiated than KIR+CD8+ T cells. In HCV‐infected patients, their content in perforin was low and similar to that observed in NKG2A−CD8+ T cells; this scenario was not observed in healthy subjects and HBV‐infected patients. Both NKG2A and KIRs could inhibit the response of HCV‐specific CD8+ T cells ex vivo. Conclusion: These results support the concept that an accumulation in the liver parenchyma of NKR+CD8+ T cells that have functional alterations could be responsible for liver lesions. They provide novel insights into the complexity of liver‐infiltrating CD8+ T cells in chronic hepatitis C and reveal that distinct subsets of antigen‐experienced CD8+ T cells are differentially sensitive to the pervasive influence of HCV (HEPATOLOGY 2007.)</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>17668887</pmid><doi>10.1002/hep.21850</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Biological and medical sciences Case-Control Studies CD8-Positive T-Lymphocytes - cytology CD8-Positive T-Lymphocytes - metabolism CD8-Positive T-Lymphocytes - physiology Female Gastroenterology. Liver. Pancreas. Abdomen Hepatitis B virus Hepatitis C virus Hepatitis C, Chronic - immunology Hepatitis C, Chronic - pathology Histocompatibility Antigens Class I - metabolism Human viral diseases Humans Infectious diseases Liver - immunology Liver - pathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Middle Aged NK Cell Lectin-Like Receptor Subfamily C Perforin - metabolism Phenotype Receptors, Immunologic - metabolism Receptors, KIR2DL1 - metabolism Receptors, KIR2DL3 - metabolism Receptors, Natural Killer Cell Viral diseases Viral hepatitis |
| title | Features and distribution of CD8 T cells with human leukocyte antigen class I–specific receptor expression in chronic hepatitis C |
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