Innate immune response and hepatic inflammation
dc.contributor.author | Szabo, Gyongyi | |
dc.contributor.author | Mandrekar, Pranoti | |
dc.contributor.author | Dolganiuc, Angela | |
dc.date | 2022-08-11T08:08:37.000 | |
dc.date.accessioned | 2022-08-23T16:01:32Z | |
dc.date.available | 2022-08-23T16:01:32Z | |
dc.date.issued | 2007-11-06 | |
dc.date.submitted | 2010-04-21 | |
dc.identifier.citation | Semin Liver Dis. 2007 Nov;27(4):339-50. <a href="http://dx.doi.org/10.1055/s-2007-991511">Link to article on publisher's site</a> | |
dc.identifier.issn | 0272-8087 (Linking) | |
dc.identifier.doi | 10.1055/s-2007-991511 | |
dc.identifier.pmid | 17979071 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/31149 | |
dc.description.abstract | Inflammation is a pathogenic component of various types of acute and chronic liver diseases, and it contributes to progressive liver damage and fibrosis. Cells of the innate immune system initiate and maintain hepatic inflammation though mediator production as a result of their activation by pathogen-derived products recognized by pattern recognition receptors. Innate immune cells, particularly dendritic cells, have a pivotal role in sensing pathogens and initiating adaptive immune responses by activation and regulation of T-lymphocyte responses. Although the liver provides a "tolerogenic" immune environment for antigen-specific T-cells, activation of Kupffer cells, recruited macrophages, and inflammatory cells results in production of cytokines and chemokines that can lead to prolonged inflammation, hepatocyte damage, and/or cholestasis. The specificity of Toll-like receptors and the mechanisms of innate immune cell activation are discussed in relation to acute and chronic liver injury including viral, alcoholic, nonalcoholic, and drug-induced hepatitis. | |
dc.language.iso | en_US | |
dc.relation | <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17979071&dopt=Abstract">Link to Article in PubMed</a> | |
dc.relation.url | http://dx.doi.org/10.1055/s-2007-991511 | |
dc.subject | Animals | |
dc.subject | Cytokines | |
dc.subject | Humans | |
dc.subject | Immunity, Innate | |
dc.subject | Inflammation | |
dc.subject | Liver | |
dc.subject | Liver Diseases | |
dc.subject | Models, Biological | |
dc.subject | Gastroenterology | |
dc.subject | Hepatology | |
dc.subject | Immunology and Infectious Disease | |
dc.title | Innate immune response and hepatic inflammation | |
dc.type | Journal Article | |
dc.source.journaltitle | Seminars in liver disease | |
dc.source.volume | 27 | |
dc.source.issue | 4 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/gastroenterology_pp/73 | |
dc.identifier.contextkey | 1282372 | |
html.description.abstract | <p>Inflammation is a pathogenic component of various types of acute and chronic liver diseases, and it contributes to progressive liver damage and fibrosis. Cells of the innate immune system initiate and maintain hepatic inflammation though mediator production as a result of their activation by pathogen-derived products recognized by pattern recognition receptors. Innate immune cells, particularly dendritic cells, have a pivotal role in sensing pathogens and initiating adaptive immune responses by activation and regulation of T-lymphocyte responses. Although the liver provides a "tolerogenic" immune environment for antigen-specific T-cells, activation of Kupffer cells, recruited macrophages, and inflammatory cells results in production of cytokines and chemokines that can lead to prolonged inflammation, hepatocyte damage, and/or cholestasis. The specificity of Toll-like receptors and the mechanisms of innate immune cell activation are discussed in relation to acute and chronic liver injury including viral, alcoholic, nonalcoholic, and drug-induced hepatitis.</p> | |
dc.identifier.submissionpath | gastroenterology_pp/73 | |
dc.contributor.department | Department of Medicine, Rheumatology Division | |
dc.contributor.department | Department of Medicine, Division of Gastroenterology | |
dc.source.pages | 339-50 |