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dc.contributor.authorSzabo, Gyongyi
dc.contributor.authorMandrekar, Pranoti
dc.contributor.authorDolganiuc, Angela
dc.date2022-08-11T08:08:37.000
dc.date.accessioned2022-08-23T16:01:32Z
dc.date.available2022-08-23T16:01:32Z
dc.date.issued2007-11-06
dc.date.submitted2010-04-21
dc.identifier.citationSemin 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.issn0272-8087 (Linking)
dc.identifier.doi10.1055/s-2007-991511
dc.identifier.pmid17979071
dc.identifier.urihttp://hdl.handle.net/20.500.14038/31149
dc.description.abstractInflammation 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.isoen_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.urlhttp://dx.doi.org/10.1055/s-2007-991511
dc.subjectAnimals
dc.subjectCytokines
dc.subjectHumans
dc.subjectImmunity, Innate
dc.subjectInflammation
dc.subjectLiver
dc.subjectLiver Diseases
dc.subjectModels, Biological
dc.subjectGastroenterology
dc.subjectHepatology
dc.subjectImmunology and Infectious Disease
dc.titleInnate immune response and hepatic inflammation
dc.typeJournal Article
dc.source.journaltitleSeminars in liver disease
dc.source.volume27
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gastroenterology_pp/73
dc.identifier.contextkey1282372
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.submissionpathgastroenterology_pp/73
dc.contributor.departmentDepartment of Medicine, Rheumatology Division
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology
dc.source.pages339-50


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