Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis

Autores
Chackelevicius, Carla Melisa; Gambaro, Sabrina Eliana; Tiribelli, Claudio; Rosso, Natalia
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD encompasses a wide histological spectrum ranging from benign simple steatosis to non-Alcoholic steatohepatitis (NASH). Sustained inflammation in the liver is critical in this process. Hepatic macrophages, including liver resident macropaghes (Kupffer cells), monocytes infiltrating the injured liver, as well as specific lymphocytes subsets play a pivotal role in the initiation and perpetuation of the inflammatory response, with a major deleterious impact on the progression of fatty liver to fibrosis. During the last years, Th17 cells have been involved in the development of inflammation not only in liver but also in other organs, such as adipose tissue or lung. Differentiation of a naïve T cell into a Th17 cell leads to pro-inflammatory cytokine and chemokine production with subsequent myeloid cell recruitment to the inflamed tissue. Th17 response can be mitigated by T regulatory cells that secrete anti-inflammatory cytokines. Both T cell subsets need TGF-β for their differentiation and a characteristic plasticity in their phenotype may render them new therapeutic targets. In this review, we discuss the role of the Th17 pathway in NAFLD progression to NASH and to liver fibrosis analyzing different animal models of liver injury and human studies.
Fil: Chackelevicius, Carla Melisa. Fondazione Italiana Fegato; Italia
Fil: Gambaro, Sabrina Eliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; Argentina
Fil: Tiribelli, Claudio. Fondazione Italiana Fegato; Italia
Fil: Rosso, Natalia. Fondazione Italiana Fegato; Italia
Materia
INFLAMMATION
INTERLEUKIN-17
NON-ALCOHOLIC STEATOHEPATITIS
NONALCOHOLIC FATTY LIVER DISEASE
TH17
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/62898
Acceder
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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitisChackelevicius, Carla MelisaGambaro, Sabrina ElianaTiribelli, ClaudioRosso, NataliaINFLAMMATIONINTERLEUKIN-17NON-ALCOHOLIC STEATOHEPATITISNONALCOHOLIC FATTY LIVER DISEASETH17https://purl.org/becyt/ford/3.4https://purl.org/becyt/ford/3The nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD encompasses a wide histological spectrum ranging from benign simple steatosis to non-Alcoholic steatohepatitis (NASH). Sustained inflammation in the liver is critical in this process. Hepatic macrophages, including liver resident macropaghes (Kupffer cells), monocytes infiltrating the injured liver, as well as specific lymphocytes subsets play a pivotal role in the initiation and perpetuation of the inflammatory response, with a major deleterious impact on the progression of fatty liver to fibrosis. During the last years, Th17 cells have been involved in the development of inflammation not only in liver but also in other organs, such as adipose tissue or lung. Differentiation of a naïve T cell into a Th17 cell leads to pro-inflammatory cytokine and chemokine production with subsequent myeloid cell recruitment to the inflamed tissue. Th17 response can be mitigated by T regulatory cells that secrete anti-inflammatory cytokines. Both T cell subsets need TGF-β for their differentiation and a characteristic plasticity in their phenotype may render them new therapeutic targets. In this review, we discuss the role of the Th17 pathway in NAFLD progression to NASH and to liver fibrosis analyzing different animal models of liver injury and human studies.Fil: Chackelevicius, Carla Melisa. Fondazione Italiana Fegato; ItaliaFil: Gambaro, Sabrina Eliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; ArgentinaFil: Tiribelli, Claudio. Fondazione Italiana Fegato; ItaliaFil: Rosso, Natalia. Fondazione Italiana Fegato; ItaliaBaishideng Publishing Group2016-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/62898Chackelevicius, Carla Melisa; Gambaro, Sabrina Eliana; Tiribelli, Claudio; Rosso, Natalia; Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis; Baishideng Publishing Group; World Journal of Gastroenterology; 22; 41; 11-2016; 9096-91031007-93272219-2840CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.3748/wjg.v22.i41.9096info:eu-repo/semantics/altIdentifier/url/https://www.wjgnet.com/1007-9327/full/v22/i41/9096.htminfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:03:02Zoai:ri.conicet.gov.ar:11336/62898instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:03:02.689CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis
title Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis
spellingShingle Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis
Chackelevicius, Carla Melisa
INFLAMMATION
INTERLEUKIN-17
NON-ALCOHOLIC STEATOHEPATITIS
NONALCOHOLIC FATTY LIVER DISEASE
TH17
title_short Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis
title_full Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis
title_fullStr Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis
title_full_unstemmed Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis
title_sort Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis
dc.creator.none.fl_str_mv Chackelevicius, Carla Melisa
Gambaro, Sabrina Eliana
Tiribelli, Claudio
Rosso, Natalia
author Chackelevicius, Carla Melisa
author_facet Chackelevicius, Carla Melisa
Gambaro, Sabrina Eliana
Tiribelli, Claudio
Rosso, Natalia
author_role author
author2 Gambaro, Sabrina Eliana
Tiribelli, Claudio
Rosso, Natalia
author2_role author
author
author
dc.subject.none.fl_str_mv INFLAMMATION
INTERLEUKIN-17
NON-ALCOHOLIC STEATOHEPATITIS
NONALCOHOLIC FATTY LIVER DISEASE
TH17
topic INFLAMMATION
INTERLEUKIN-17
NON-ALCOHOLIC STEATOHEPATITIS
NONALCOHOLIC FATTY LIVER DISEASE
TH17
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.4
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD encompasses a wide histological spectrum ranging from benign simple steatosis to non-Alcoholic steatohepatitis (NASH). Sustained inflammation in the liver is critical in this process. Hepatic macrophages, including liver resident macropaghes (Kupffer cells), monocytes infiltrating the injured liver, as well as specific lymphocytes subsets play a pivotal role in the initiation and perpetuation of the inflammatory response, with a major deleterious impact on the progression of fatty liver to fibrosis. During the last years, Th17 cells have been involved in the development of inflammation not only in liver but also in other organs, such as adipose tissue or lung. Differentiation of a naïve T cell into a Th17 cell leads to pro-inflammatory cytokine and chemokine production with subsequent myeloid cell recruitment to the inflamed tissue. Th17 response can be mitigated by T regulatory cells that secrete anti-inflammatory cytokines. Both T cell subsets need TGF-β for their differentiation and a characteristic plasticity in their phenotype may render them new therapeutic targets. In this review, we discuss the role of the Th17 pathway in NAFLD progression to NASH and to liver fibrosis analyzing different animal models of liver injury and human studies.
Fil: Chackelevicius, Carla Melisa. Fondazione Italiana Fegato; Italia
Fil: Gambaro, Sabrina Eliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; Argentina
Fil: Tiribelli, Claudio. Fondazione Italiana Fegato; Italia
Fil: Rosso, Natalia. Fondazione Italiana Fegato; Italia
description The nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD encompasses a wide histological spectrum ranging from benign simple steatosis to non-Alcoholic steatohepatitis (NASH). Sustained inflammation in the liver is critical in this process. Hepatic macrophages, including liver resident macropaghes (Kupffer cells), monocytes infiltrating the injured liver, as well as specific lymphocytes subsets play a pivotal role in the initiation and perpetuation of the inflammatory response, with a major deleterious impact on the progression of fatty liver to fibrosis. During the last years, Th17 cells have been involved in the development of inflammation not only in liver but also in other organs, such as adipose tissue or lung. Differentiation of a naïve T cell into a Th17 cell leads to pro-inflammatory cytokine and chemokine production with subsequent myeloid cell recruitment to the inflamed tissue. Th17 response can be mitigated by T regulatory cells that secrete anti-inflammatory cytokines. Both T cell subsets need TGF-β for their differentiation and a characteristic plasticity in their phenotype may render them new therapeutic targets. In this review, we discuss the role of the Th17 pathway in NAFLD progression to NASH and to liver fibrosis analyzing different animal models of liver injury and human studies.
publishDate 2016
dc.date.none.fl_str_mv 2016-11
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/62898
Chackelevicius, Carla Melisa; Gambaro, Sabrina Eliana; Tiribelli, Claudio; Rosso, Natalia; Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis; Baishideng Publishing Group; World Journal of Gastroenterology; 22; 41; 11-2016; 9096-9103
1007-9327
2219-2840
CONICET Digital
CONICET
url http://hdl.handle.net/11336/62898
identifier_str_mv Chackelevicius, Carla Melisa; Gambaro, Sabrina Eliana; Tiribelli, Claudio; Rosso, Natalia; Th17 involvement in nonalcoholic fatty liver disease progression to non-Alcoholic steatohepatitis; Baishideng Publishing Group; World Journal of Gastroenterology; 22; 41; 11-2016; 9096-9103
1007-9327
2219-2840
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.3748/wjg.v22.i41.9096
info:eu-repo/semantics/altIdentifier/url/https://www.wjgnet.com/1007-9327/full/v22/i41/9096.htm
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Baishideng Publishing Group
publisher.none.fl_str_mv Baishideng Publishing Group
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1842269780339326976
score 13.13397

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