Intrahepatic mRNA Expression of FAS, FASL, and FOXP3 Genes Is Associated with the Pathophysiology of Chronic HCV Infection
This study aimed to evaluate the relative mRNA expression of Fas receptor (FAS), Fas ligand (FASL), and forkhead box protein 3 (FOXP3) in liver biopsy specimens obtained from patients with viral and non-viral chronic hepatitis and correlate their expression with the fibrosis stage. A total of 51 liv...
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| Veröffentlicht in: | PloS one 2016-05, Vol.11 (5), p.e0156604-e0156604 |
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| creator | Amoras, Ednelza da Silva Graça Gomes, Samara Tatielle Monteiro Freitas, Felipe Bonfim Santana, Bárbara Brasil Ishak, Geraldo Ferreira de Araújo, Marialva Tereza Demachki, Sâmia Conde, Simone Regina Souza da Silva Ishak, Marluísa de Oliveira Guimarães Ishak, Ricardo Vallinoto, Antonio Carlos Rosário |
| description | This study aimed to evaluate the relative mRNA expression of Fas receptor (FAS), Fas ligand (FASL), and forkhead box protein 3 (FOXP3) in liver biopsy specimens obtained from patients with viral and non-viral chronic hepatitis and correlate their expression with the fibrosis stage. A total of 51 liver biopsy specimens obtained from HBV (n = 6), HCV (n = 28), and non-viral hepatic disease (NVHD) (n = 9) patients and from individuals with normal liver histology (n = 8) (control-CT) were analyzed. Quantifications of the target genes were assessed using qPCR, and liver biopsies according to the METAVIR classification. The mRNA expression levels of FAS and FASL were lower in the CT group compared to the groups of patients. The increase in the mRNA expression of FAS and FASL was correlated with higher levels of inflammation and disease progression, followed by a decline in tissues with cirrhosis, and it was also associated with increased levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Higher mRNA expression of FOXP3 was observed in the HCV and NVHD groups, with the peak observed among patients with cirrhosis. The increased FOXP3 mRNA expression was positively correlated with increased FAS and FASL mRNA expression and the AST and ALT levels in all patients.
These results suggest that regardless of the cause, the course of chronic liver disease may be modulated by the analyzed genes and correlated with an increase in regulatory T cells during the liver damage followed by hepatocyte destruction by Fas/FasL system and subsequent non specific lymphocytic infiltrate accumulation. |
| doi_str_mv | 10.1371/journal.pone.0156604 |
| format | Article |
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These results suggest that regardless of the cause, the course of chronic liver disease may be modulated by the analyzed genes and correlated with an increase in regulatory T cells during the liver damage followed by hepatocyte destruction by Fas/FasL system and subsequent non specific lymphocytic infiltrate accumulation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0156604</identifier><identifier>PMID: 27243827</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alanine ; Alanine transaminase ; Alanine Transaminase - metabolism ; Apoptosis ; Aspartate aminotransferase ; Aspartate Aminotransferases - metabolism ; Biology and Life Sciences ; Biopsy ; CD4 Lymphocyte Count ; Chronic illnesses ; Chronic infection ; Cirrhosis ; Correlation analysis ; Cytokines ; Development and progression ; Fas Ligand Protein - genetics ; fas Receptor - genetics ; FasL protein ; Fibrosis ; Forkhead protein ; Forkhead Transcription Factors - genetics ; Foxp3 protein ; Gene expression ; Genes ; Genetic aspects ; Health aspects ; Health sciences ; Hepacivirus - immunology ; Hepatitis ; Hepatitis B virus ; Hepatitis C ; Hepatitis C virus ; Hepatitis C, Chronic - physiopathology ; Hepatocytes ; Hepatocytes - metabolism ; Hepatology ; Histology ; Humans ; Immunoregulation ; Infections ; Laboratories ; Ligands ; Liver ; Liver - metabolism ; Liver cirrhosis ; Liver Cirrhosis - pathology ; Liver diseases ; Lymphocytes ; Lymphocytes T ; Medicine ; Medicine and health sciences ; Membrane proteins ; Messenger RNA ; Patients ; Polymerase Chain Reaction ; Properties ; Proteins ; RNA, Messenger - biosynthesis ; RNA, Messenger - genetics ; Rodents ; T cell receptors ; T-Lymphocytes, Regulatory - cytology ; T-Lymphocytes, Regulatory - immunology ; Virology ; Viruses</subject><ispartof>PloS one, 2016-05, Vol.11 (5), p.e0156604-e0156604</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Amoras et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Amoras et al 2016 Amoras et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-56dbdf8416349c1acbcad3c5c93f5dd2b4220bdee36993c33853a857bb7f0ead3</citedby><cites>FETCH-LOGICAL-c725t-56dbdf8416349c1acbcad3c5c93f5dd2b4220bdee36993c33853a857bb7f0ead3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4887037/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4887037/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27243827$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Amoras, Ednelza da Silva Graça</creatorcontrib><creatorcontrib>Gomes, Samara Tatielle Monteiro</creatorcontrib><creatorcontrib>Freitas, Felipe Bonfim</creatorcontrib><creatorcontrib>Santana, Bárbara Brasil</creatorcontrib><creatorcontrib>Ishak, Geraldo</creatorcontrib><creatorcontrib>Ferreira de Araújo, Marialva Tereza</creatorcontrib><creatorcontrib>Demachki, Sâmia</creatorcontrib><creatorcontrib>Conde, Simone Regina Souza da Silva</creatorcontrib><creatorcontrib>Ishak, Marluísa de Oliveira Guimarães</creatorcontrib><creatorcontrib>Ishak, Ricardo</creatorcontrib><creatorcontrib>Vallinoto, Antonio Carlos Rosário</creatorcontrib><title>Intrahepatic mRNA Expression of FAS, FASL, and FOXP3 Genes Is Associated with the Pathophysiology of Chronic HCV Infection</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>This study aimed to evaluate the relative mRNA expression of Fas receptor (FAS), Fas ligand (FASL), and forkhead box protein 3 (FOXP3) in liver biopsy specimens obtained from patients with viral and non-viral chronic hepatitis and correlate their expression with the fibrosis stage. A total of 51 liver biopsy specimens obtained from HBV (n = 6), HCV (n = 28), and non-viral hepatic disease (NVHD) (n = 9) patients and from individuals with normal liver histology (n = 8) (control-CT) were analyzed. Quantifications of the target genes were assessed using qPCR, and liver biopsies according to the METAVIR classification. The mRNA expression levels of FAS and FASL were lower in the CT group compared to the groups of patients. The increase in the mRNA expression of FAS and FASL was correlated with higher levels of inflammation and disease progression, followed by a decline in tissues with cirrhosis, and it was also associated with increased levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Higher mRNA expression of FOXP3 was observed in the HCV and NVHD groups, with the peak observed among patients with cirrhosis. The increased FOXP3 mRNA expression was positively correlated with increased FAS and FASL mRNA expression and the AST and ALT levels in all patients.
These results suggest that regardless of the cause, the course of chronic liver disease may be modulated by the analyzed genes and correlated with an increase in regulatory T cells during the liver damage followed by hepatocyte destruction by Fas/FasL system and subsequent non specific lymphocytic infiltrate accumulation.</description><subject>Alanine</subject><subject>Alanine transaminase</subject><subject>Alanine Transaminase - metabolism</subject><subject>Apoptosis</subject><subject>Aspartate aminotransferase</subject><subject>Aspartate Aminotransferases - metabolism</subject><subject>Biology and Life Sciences</subject><subject>Biopsy</subject><subject>CD4 Lymphocyte Count</subject><subject>Chronic illnesses</subject><subject>Chronic infection</subject><subject>Cirrhosis</subject><subject>Correlation analysis</subject><subject>Cytokines</subject><subject>Development and progression</subject><subject>Fas Ligand Protein - genetics</subject><subject>fas Receptor - genetics</subject><subject>FasL protein</subject><subject>Fibrosis</subject><subject>Forkhead protein</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Foxp3 protein</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Health sciences</subject><subject>Hepacivirus - immunology</subject><subject>Hepatitis</subject><subject>Hepatitis B virus</subject><subject>Hepatitis C</subject><subject>Hepatitis C virus</subject><subject>Hepatitis C, Chronic - physiopathology</subject><subject>Hepatocytes</subject><subject>Hepatocytes - metabolism</subject><subject>Hepatology</subject><subject>Histology</subject><subject>Humans</subject><subject>Immunoregulation</subject><subject>Infections</subject><subject>Laboratories</subject><subject>Ligands</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver diseases</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Medicine</subject><subject>Medicine and health sciences</subject><subject>Membrane proteins</subject><subject>Messenger RNA</subject><subject>Patients</subject><subject>Polymerase Chain Reaction</subject><subject>Properties</subject><subject>Proteins</subject><subject>RNA, Messenger - biosynthesis</subject><subject>RNA, Messenger - genetics</subject><subject>Rodents</subject><subject>T cell receptors</subject><subject>T-Lymphocytes, Regulatory - cytology</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Virology</subject><subject>Viruses</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk-Fr1DAUwIsobk7_A9HAQBR2Z9I0TfpFOI7dVji8senwW0jT12uPXlObVnf-9aZeN64yUAppSH_vl_S9PM97TfCUUE4-bkzXVKqc1qaCKSYsDHHwxDsmEfUnoY_p04P5kffC2g3GjIowfO4d-dwPqPD5sfcrrtpG5VCrttBoe_15hs7v6gasLUyFTIYWs5uzflieIVWlaLH6dkXRBVRgUWzRzFqjC9VCin4WbY7aHNCVanNT5ztnKM1610vmeWMq57-c36K4ykC3zv7Se5ap0sKr4X3ifV2cf5lfTpari3g-W04091k7YWGapJkISEiDSBOlE61SqpmOaMbS1E8C38dJCkDDKKKaUsGoEownCc8wOPTEe7v31qWxckiblYRHPueU0MgR8Z5IjdrIuim2qtlJowr5Z8E0a6kal58SJCSJ5pEGwQQOMElExiOc-UBSUEmSCef6NOzWJVtINfT5LUfS8ZeqyOXa_JCBEBxT7gTvB0FjvndgW7ktrIayVBWYzp1bYFdETAX9N8ojykJBCXbo6V_o44kYqLVy_1pUmXFH1L1UzgJGuQgZ66npI5R7UtgW2l3HrHDro4APowDHtHDXrlVnrYxvrv-fXd2O2XcHbA6qbHNryq6_XXYMBntQN8baBrKHehAs-266z4bsu0kO3eTC3hzW8iHovn3ob1ksGUo</recordid><startdate>20160531</startdate><enddate>20160531</enddate><creator>Amoras, Ednelza da Silva Graça</creator><creator>Gomes, Samara Tatielle Monteiro</creator><creator>Freitas, Felipe Bonfim</creator><creator>Santana, Bárbara Brasil</creator><creator>Ishak, Geraldo</creator><creator>Ferreira de Araújo, Marialva Tereza</creator><creator>Demachki, Sâmia</creator><creator>Conde, Simone Regina Souza da Silva</creator><creator>Ishak, Marluísa de Oliveira Guimarães</creator><creator>Ishak, Ricardo</creator><creator>Vallinoto, Antonio Carlos Rosário</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20160531</creationdate><title>Intrahepatic mRNA Expression of FAS, FASL, and FOXP3 Genes Is Associated with the Pathophysiology of Chronic HCV Infection</title><author>Amoras, Ednelza da Silva Graça ; Gomes, Samara Tatielle Monteiro ; Freitas, Felipe Bonfim ; Santana, Bárbara Brasil ; Ishak, Geraldo ; Ferreira de Araújo, Marialva Tereza ; Demachki, Sâmia ; Conde, Simone Regina Souza da Silva ; Ishak, Marluísa de Oliveira Guimarães ; Ishak, Ricardo ; Vallinoto, Antonio Carlos Rosário</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c725t-56dbdf8416349c1acbcad3c5c93f5dd2b4220bdee36993c33853a857bb7f0ead3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Alanine</topic><topic>Alanine transaminase</topic><topic>Alanine Transaminase - 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metabolism</topic><topic>Hepatology</topic><topic>Histology</topic><topic>Humans</topic><topic>Immunoregulation</topic><topic>Infections</topic><topic>Laboratories</topic><topic>Ligands</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Liver cirrhosis</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver diseases</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Medicine</topic><topic>Medicine and health sciences</topic><topic>Membrane proteins</topic><topic>Messenger RNA</topic><topic>Patients</topic><topic>Polymerase Chain Reaction</topic><topic>Properties</topic><topic>Proteins</topic><topic>RNA, Messenger - biosynthesis</topic><topic>RNA, Messenger - genetics</topic><topic>Rodents</topic><topic>T cell receptors</topic><topic>T-Lymphocytes, Regulatory - cytology</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>Virology</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Amoras, Ednelza da Silva Graça</creatorcontrib><creatorcontrib>Gomes, Samara Tatielle Monteiro</creatorcontrib><creatorcontrib>Freitas, Felipe Bonfim</creatorcontrib><creatorcontrib>Santana, Bárbara Brasil</creatorcontrib><creatorcontrib>Ishak, Geraldo</creatorcontrib><creatorcontrib>Ferreira de Araújo, Marialva Tereza</creatorcontrib><creatorcontrib>Demachki, Sâmia</creatorcontrib><creatorcontrib>Conde, Simone Regina Souza da Silva</creatorcontrib><creatorcontrib>Ishak, Marluísa de Oliveira Guimarães</creatorcontrib><creatorcontrib>Ishak, Ricardo</creatorcontrib><creatorcontrib>Vallinoto, Antonio Carlos Rosário</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Amoras, Ednelza da Silva Graça</au><au>Gomes, Samara Tatielle Monteiro</au><au>Freitas, Felipe Bonfim</au><au>Santana, Bárbara Brasil</au><au>Ishak, Geraldo</au><au>Ferreira de Araújo, Marialva Tereza</au><au>Demachki, Sâmia</au><au>Conde, Simone Regina Souza da Silva</au><au>Ishak, Marluísa de Oliveira Guimarães</au><au>Ishak, Ricardo</au><au>Vallinoto, Antonio Carlos Rosário</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intrahepatic mRNA Expression of FAS, FASL, and FOXP3 Genes Is Associated with the Pathophysiology of Chronic HCV Infection</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-05-31</date><risdate>2016</risdate><volume>11</volume><issue>5</issue><spage>e0156604</spage><epage>e0156604</epage><pages>e0156604-e0156604</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>This study aimed to evaluate the relative mRNA expression of Fas receptor (FAS), Fas ligand (FASL), and forkhead box protein 3 (FOXP3) in liver biopsy specimens obtained from patients with viral and non-viral chronic hepatitis and correlate their expression with the fibrosis stage. A total of 51 liver biopsy specimens obtained from HBV (n = 6), HCV (n = 28), and non-viral hepatic disease (NVHD) (n = 9) patients and from individuals with normal liver histology (n = 8) (control-CT) were analyzed. Quantifications of the target genes were assessed using qPCR, and liver biopsies according to the METAVIR classification. The mRNA expression levels of FAS and FASL were lower in the CT group compared to the groups of patients. The increase in the mRNA expression of FAS and FASL was correlated with higher levels of inflammation and disease progression, followed by a decline in tissues with cirrhosis, and it was also associated with increased levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Higher mRNA expression of FOXP3 was observed in the HCV and NVHD groups, with the peak observed among patients with cirrhosis. The increased FOXP3 mRNA expression was positively correlated with increased FAS and FASL mRNA expression and the AST and ALT levels in all patients.
These results suggest that regardless of the cause, the course of chronic liver disease may be modulated by the analyzed genes and correlated with an increase in regulatory T cells during the liver damage followed by hepatocyte destruction by Fas/FasL system and subsequent non specific lymphocytic infiltrate accumulation.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27243827</pmid><doi>10.1371/journal.pone.0156604</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-05, Vol.11 (5), p.e0156604-e0156604 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1792773139 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Alanine Alanine transaminase Alanine Transaminase - metabolism Apoptosis Aspartate aminotransferase Aspartate Aminotransferases - metabolism Biology and Life Sciences Biopsy CD4 Lymphocyte Count Chronic illnesses Chronic infection Cirrhosis Correlation analysis Cytokines Development and progression Fas Ligand Protein - genetics fas Receptor - genetics FasL protein Fibrosis Forkhead protein Forkhead Transcription Factors - genetics Foxp3 protein Gene expression Genes Genetic aspects Health aspects Health sciences Hepacivirus - immunology Hepatitis Hepatitis B virus Hepatitis C Hepatitis C virus Hepatitis C, Chronic - physiopathology Hepatocytes Hepatocytes - metabolism Hepatology Histology Humans Immunoregulation Infections Laboratories Ligands Liver Liver - metabolism Liver cirrhosis Liver Cirrhosis - pathology Liver diseases Lymphocytes Lymphocytes T Medicine Medicine and health sciences Membrane proteins Messenger RNA Patients Polymerase Chain Reaction Properties Proteins RNA, Messenger - biosynthesis RNA, Messenger - genetics Rodents T cell receptors T-Lymphocytes, Regulatory - cytology T-Lymphocytes, Regulatory - immunology Virology Viruses |
| title | Intrahepatic mRNA Expression of FAS, FASL, and FOXP3 Genes Is Associated with the Pathophysiology of Chronic HCV Infection |
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