{"id":{"repo_id":"aachen","oai_identifier":"oai:publications.rwth-aachen.de:61519"},"canonical_url":"https://search.dev.ndltd.org/etd/aachen/oai:publications.rwth-aachen.de:61519","repository":{"repo_id":"aachen","name":"RWTH Aachen University","base_url":"https://publications.rwth-aachen.de/oai2d"},"display":{"title":"Untersuchungen zur Rolle von Zytokinen bei der Beta-2-Mikroglobulin-Synthese in verschiedenen humanen Zelltypen","abstract":"Background. Proinflammatory monocytic cytokines such as interleukin-1 (IL-1), tumour necrosis factor-alpha (TNF-alpha) and IL-6 have been incriminated in the pathogenesis of elevated beta-2-microglobulin (beta-2-M) serum concentrations in patients undergoing haemodialysis with so-called bioincompatible dialyser membranes. However, neither the source of the elevated serum beta-2-M nor the precise role of monocytic cytokines in the expression of the beta-2-M gene have been elucidated conclusively. The aim of this study was to evaluate whether monoytic cytokines, and in particular IL-6, are regulators of beta-2-M gene expression in human hepatoma cells, T-lymphocytes and monocytes. Methods. HepG2 and HuH7 human hepatoma cells, Jurkat T-cells, monocytic MonoMac6 cells, primary human monocytes and synoviocytes were stimulated with IL-1-beta, IL-6, interferon-alpha (IFN-alpha), IFN-gamma or conditioned media from lipopolysaccharide (LPS)-treated monocytes. Expression of beta-2-M mRNA was analysed by Northern blotting, beta-2-M protein synthesis was determined by metabolic labelling and immunoprecipitation, and beta-2-M secretion was measured by an enzyme-linked immunosorbent assay (ELISA). Results. In all cell types tested, IFN-gamma and, to a lesser extent, IFN-alpha stimulated gene expression of beta-2-M resulting in an increased synthesis and secretion of beta-2-M protein. Neither IL-1-beta and IL-6 nor supernatants from LPS-treated monocytes were capable of inducing beta-2-M gene expression, with the exception of a small increase in HuH7 hepatoma cells upon IL-1-beta treatment. Conclusions. The present study provides evidence that interferons are important regulators of beta-2-M expression. It also shows that proinflammatory monocytic cytokines do not modulate directly the expression of beta-2-M in cells of hepatic, monocytic and T-lymphocytic origin. Whether they are other inflammatory influences to the bioincompability of dialyser membranes is discussed in this study.","abstract_html":"Background. Proinflammatory monocytic cytokines such as interleukin-1 (IL-1), tumour necrosis factor-alpha (TNF-alpha) and IL-6 have been incriminated in the pathogenesis of elevated beta-2-microglobulin (beta-2-M) serum concentrations in patients undergoing haemodialysis with so-called bioincompatible dialyser membranes. However, neither the source of the elevated serum beta-2-M nor the precise role of monocytic cytokines in the expression of the beta-2-M gene have been elucidated conclusively. The aim of this study was to evaluate whether monoytic cytokines, and in particular IL-6, are regulators of beta-2-M gene expression in human hepatoma cells, T-lymphocytes and monocytes. Methods. HepG2 and HuH7 human hepatoma cells, Jurkat T-cells, monocytic MonoMac6 cells, primary human monocytes and synoviocytes were stimulated with IL-1-beta, IL-6, interferon-alpha (IFN-alpha), IFN-gamma or conditioned media from lipopolysaccharide (LPS)-treated monocytes. Expression of beta-2-M mRNA was analysed by Northern blotting, beta-2-M protein synthesis was determined by metabolic labelling and immunoprecipitation, and beta-2-M secretion was measured by an enzyme-linked immunosorbent assay (ELISA). Results. In all cell types tested, IFN-gamma and, to a lesser extent, IFN-alpha stimulated gene expression of beta-2-M resulting in an increased synthesis and secretion of beta-2-M protein. Neither IL-1-beta and IL-6 nor supernatants from LPS-treated monocytes were capable of inducing beta-2-M gene expression, with the exception of a small increase in HuH7 hepatoma cells upon IL-1-beta treatment. Conclusions. The present study provides evidence that interferons are important regulators of beta-2-M expression. It also shows that proinflammatory monocytic cytokines do not modulate directly the expression of beta-2-M in cells of hepatic, monocytic and T-lymphocytic origin. Whether they are other inflammatory influences to the bioincompability of dialyser membranes is discussed in this study.","abstract_has_math":false,"creators":["Vraetz, Thomas"],"institution":"Publikationsserver der RWTH Aachen University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Graeve, Lutz"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2006,"date_issued":"2006","date_published":"2006","updated_at":"2026-07-30T19:43:10Z","subjects":["info:eu-repo/classification/ddc/610","Amyloidose","Mikroglobulin <beta-2->","Dialyse","Interleukin 6","Interleukin 1","Interferon <gamma->","Interferon","Interferon <alpha->","Medizin","Bioinkompatibilität","Zytokine","Hämodialyse","Beta-2-Mikroglobulin","bioincompatibility","cytokines","haemodialysis","beta-2-microglobulin","amyloidosis"],"languages":["ger"],"rights":["info:eu-repo/semantics/openAccess"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-123177%22"],"render_values":[{"text":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-123177%22","href":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-123177%22","code":true}]}]},"links":{"outbound_url":"https://publications.rwth-aachen.de/record/61519","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Graeve, Lutz"]},{"key":"dc:creator","label":"Author","values":["Vraetz, Thomas"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:coverage","label":"Dc Coverage","values":["DE"]},{"key":"dc:date","label":"Dc Date","values":["2006"]},{"key":"dc:publisher","label":"Institution","values":["Publikationsserver der RWTH Aachen University"]},{"key":"dc:relation","label":"Dc Relation","values":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-16410"]},{"key":"dc:type","label":"Dc Type","values":["info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["info:eu-repo/classification/ddc/610","Amyloidose","Mikroglobulin <beta-2->","Dialyse","Interleukin 6","Interleukin 1","Interferon <gamma->","Interferon","Interferon <alpha->","Medizin","Bioinkompatibilität","Zytokine","Hämodialyse","Beta-2-Mikroglobulin","bioincompatibility","cytokines","haemodialysis","beta-2-microglobulin","amyloidosis"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["ger"]},{"key":"dc:rights","label":"Dc Rights","values":["info:eu-repo/semantics/openAccess"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/record/61519","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-123177%22"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Background. Proinflammatory monocytic cytokines such as interleukin-1 (IL-1), tumour necrosis factor-alpha (TNF-alpha) and IL-6 have been incriminated in the pathogenesis of elevated beta-2-microglobulin (beta-2-M) serum concentrations in patients undergoing haemodialysis with so-called bioincompatible dialyser membranes. However, neither the source of the elevated serum beta-2-M nor the precise role of monocytic cytokines in the expression of the beta-2-M gene have been elucidated conclusively. The aim of this study was to evaluate whether monoytic cytokines, and in particular IL-6, are regulators of beta-2-M gene expression in human hepatoma cells, T-lymphocytes and monocytes. Methods. HepG2 and HuH7 human hepatoma cells, Jurkat T-cells, monocytic MonoMac6 cells, primary human monocytes and synoviocytes were stimulated with IL-1-beta, IL-6, interferon-alpha (IFN-alpha), IFN-gamma or conditioned media from lipopolysaccharide (LPS)-treated monocytes. Expression of beta-2-M mRNA was analysed by Northern blotting, beta-2-M protein synthesis was determined by metabolic labelling and immunoprecipitation, and beta-2-M secretion was measured by an enzyme-linked immunosorbent assay (ELISA). Results. In all cell types tested, IFN-gamma and, to a lesser extent, IFN-alpha stimulated gene expression of beta-2-M resulting in an increased synthesis and secretion of beta-2-M protein. Neither IL-1-beta and IL-6 nor supernatants from LPS-treated monocytes were capable of inducing beta-2-M gene expression, with the exception of a small increase in HuH7 hepatoma cells upon IL-1-beta treatment. Conclusions. The present study provides evidence that interferons are important regulators of beta-2-M expression. It also shows that proinflammatory monocytic cytokines do not modulate directly the expression of beta-2-M in cells of hepatic, monocytic and T-lymphocytic origin. Whether they are other inflammatory influences to the bioincompability of dialyser membranes is discussed in this study."]},{"key":"dc:source","label":"Dc Source","values":["Aachen : Publikationsserver der RWTH Aachen University 147 S. : Ill., graph. Darst. (2006). = Aachen, Techn. Hochsch., Diss., 2006"]},{"key":"dc:title","label":"Title","values":["Untersuchungen zur Rolle von Zytokinen bei der Beta-2-Mikroglobulin-Synthese in verschiedenen humanen Zelltypen"]}]}],"canonical_facts":{"dc:contributor":["Graeve, Lutz"],"dc:coverage":["DE"],"dc:creator":["Vraetz, Thomas"],"dc:date":["2006"],"dc:description":["Background. Proinflammatory monocytic cytokines such as interleukin-1 (IL-1), tumour necrosis factor-alpha (TNF-alpha) and IL-6 have been incriminated in the pathogenesis of elevated beta-2-microglobulin (beta-2-M) serum concentrations in patients undergoing haemodialysis with so-called bioincompatible dialyser membranes. However, neither the source of the elevated serum beta-2-M nor the precise role of monocytic cytokines in the expression of the beta-2-M gene have been elucidated conclusively. The aim of this study was to evaluate whether monoytic cytokines, and in particular IL-6, are regulators of beta-2-M gene expression in human hepatoma cells, T-lymphocytes and monocytes. Methods. HepG2 and HuH7 human hepatoma cells, Jurkat T-cells, monocytic MonoMac6 cells, primary human monocytes and synoviocytes were stimulated with IL-1-beta, IL-6, interferon-alpha (IFN-alpha), IFN-gamma or conditioned media from lipopolysaccharide (LPS)-treated monocytes. Expression of beta-2-M mRNA was analysed by Northern blotting, beta-2-M protein synthesis was determined by metabolic labelling and immunoprecipitation, and beta-2-M secretion was measured by an enzyme-linked immunosorbent assay (ELISA). Results. In all cell types tested, IFN-gamma and, to a lesser extent, IFN-alpha stimulated gene expression of beta-2-M resulting in an increased synthesis and secretion of beta-2-M protein. Neither IL-1-beta and IL-6 nor supernatants from LPS-treated monocytes were capable of inducing beta-2-M gene expression, with the exception of a small increase in HuH7 hepatoma cells upon IL-1-beta treatment. Conclusions. The present study provides evidence that interferons are important regulators of beta-2-M expression. It also shows that proinflammatory monocytic cytokines do not modulate directly the expression of beta-2-M in cells of hepatic, monocytic and T-lymphocytic origin. Whether they are other inflammatory influences to the bioincompability of dialyser membranes is discussed in this study."],"dc:identifier":["https://publications.rwth-aachen.de/record/61519","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-123177%22"],"dc:language":["ger"],"dc:publisher":["Publikationsserver der RWTH Aachen University"],"dc:relation":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-16410"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:source":["Aachen : Publikationsserver der RWTH Aachen University 147 S. : Ill., graph. Darst. (2006). = Aachen, Techn. Hochsch., Diss., 2006"],"dc:subject":["info:eu-repo/classification/ddc/610","Amyloidose","Mikroglobulin <beta-2->","Dialyse","Interleukin 6","Interleukin 1","Interferon <gamma->","Interferon","Interferon <alpha->","Medizin","Bioinkompatibilität","Zytokine","Hämodialyse","Beta-2-Mikroglobulin","bioincompatibility","cytokines","haemodialysis","beta-2-microglobulin","amyloidosis"],"dc:title":["Untersuchungen zur Rolle von Zytokinen bei der Beta-2-Mikroglobulin-Synthese in verschiedenen humanen Zelltypen"],"dc:type":["info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]},"updated_at":"2026-07-30T19:43:10Z"}