{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/20296"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/20296","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Differentiation and activation of functionally distinct macrophage populations by CSF-1 and GM-CSF","abstract":"Macrophages derived in vitro from bone marrow progenitor cells (BMDM) under the influence of CSF-1 or GM-CSF were compared for immune function. CSF-1- and GM-CSF-derived BMDM did not differ in their ability to kill L929 tumor targets or produce IL-6 and LTC$\\sb4$ in response to IFN-$\\gamma$ and LPS. CSF-1-derived BMDM secreted more TNF-$\\alpha$ and PGE$\\sb2$ at early stages of culture than did GM-CSF-derived BMDM and required only LPS stimulation to produce NO$\\sb2\\sp-$. In contrast, GM-CSF-derived BMDM secreted NO$\\sb2\\sp-$ only following treatment with IFN-$\\gamma$ plus LPS. When P815 tumor targets were used, GM-CSF-derived BMDM displayed higher basal and inducible levels of killing than CSF-1-derived BMDM and required only LPS treatment to reach full cytolytic capacity. Additionally, GM-CSF-derived BMDM showed greater listeriacidal capacity than did CSF-1-derived BMDM, particularly following IFN-$\\gamma$ plus LPS treatment. To assess immunocompetence under conditions resembling those of inflammatory sites, BMDM function was examined following treatment with PGE$\\sb2$ or in conditions of reduced L-arginine concentration. PGE$\\sb2$ (10$\\sp{-6}$-10$\\sp{-8}$ M) had no effect on BMDM ability to cytolyze L929 cells, kill intracellular Listeria, or produce NO$\\sb2\\sp-$, but GM-CSF-derived BMDM were inhibited 33% for cytolysis of K562 tumor cells. Interestingly, GM-CSF-derived BMDM were much less sensitive than CSF-1-derived BMDM for PGE$\\sb2$, but not cAMP-mediated inhibition of TNF-$\\alpha$. Arginine depletion blocked NO$\\sb2\\sp-$ production by both BMDM populations and the listeriacidal activity induced by IFN-$\\gamma$ plus LPS was abolished.","abstract_html":"Macrophages derived in vitro from bone marrow progenitor cells (BMDM) under the influence of CSF-1 or GM-CSF were compared for immune function. CSF-1- and GM-CSF-derived BMDM did not differ in their ability to kill L929 tumor targets or produce IL-6 and LTC$\\sb4$ in response to IFN-<span class=\"etd-inline-math\">&gamma;</span> and LPS. CSF-1-derived BMDM secreted more TNF-<span class=\"etd-inline-math\">&alpha;</span> and PGE$\\sb2$ at early stages of culture than did GM-CSF-derived BMDM and required only LPS stimulation to produce NO$\\sb2\\sp-$. In contrast, GM-CSF-derived BMDM secreted NO$\\sb2\\sp-$ only following treatment with IFN-<span class=\"etd-inline-math\">&gamma;</span> plus LPS. When P815 tumor targets were used, GM-CSF-derived BMDM displayed higher basal and inducible levels of killing than CSF-1-derived BMDM and required only LPS treatment to reach full cytolytic capacity. Additionally, GM-CSF-derived BMDM showed greater listeriacidal capacity than did CSF-1-derived BMDM, particularly following IFN-<span class=\"etd-inline-math\">&gamma;</span> plus LPS treatment. To assess immunocompetence under conditions resembling those of inflammatory sites, BMDM function was examined following treatment with PGE$\\sb2$ or in conditions of reduced L-arginine concentration. PGE$\\sb2$ (10$\\sp{-6}$-10$\\sp{-8}$ M) had no effect on BMDM ability to cytolyze L929 cells, kill intracellular Listeria, or produce NO$\\sb2\\sp-$, but GM-CSF-derived BMDM were inhibited 33% for cytolysis of K562 tumor cells. Interestingly, GM-CSF-derived BMDM were much less sensitive than CSF-1-derived BMDM for PGE$\\sb2$, but not cAMP-mediated inhibition of TNF-<span class=\"etd-inline-math\">&alpha;</span>. Arginine depletion blocked NO$\\sb2\\sp-$ production by both BMDM populations and the listeriacidal activity induced by IFN-<span class=\"etd-inline-math\">&gamma;</span> plus LPS was abolished.","abstract_has_math":true,"creators":["Rutherford, Mark Stephen"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Pathobiology","degree_department":null,"school":null,"contributors":["Shapiro, Stuart Z."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-05-07T12:35:11Z","date_published":"2011-05-07T12:35:11Z","updated_at":"2026-07-22T22:25:15Z","subjects":["Biology, Cell","Health Sciences, Immunology"],"languages":["eng"],"rights":["Copyright 1991 Rutherford, Mark Stephen"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9124479","(UMI)AAI9124479"],"render_values":[{"text":"AAI9124479","href":null,"code":true},{"text":"(UMI)AAI9124479","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/20296","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Shapiro, Stuart Z."]},{"key":"dc:creator","label":"Author","values":["Rutherford, Mark Stephen"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2011-05-07T12:35:11Z","10000-01-01","1991"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Pathobiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Cell","Health Sciences, Immunology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 1991 Rutherford, Mark Stephen"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9124479","(UMI)AAI9124479","http://hdl.handle.net/2142/20296"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Macrophages derived in vitro from bone marrow progenitor cells (BMDM) under the influence of CSF-1 or GM-CSF were compared for immune function. CSF-1- and GM-CSF-derived BMDM did not differ in their ability to kill L929 tumor targets or produce IL-6 and LTC$\\sb4$ in response to IFN-$\\gamma$ and LPS. CSF-1-derived BMDM secreted more TNF-$\\alpha$ and PGE$\\sb2$ at early stages of culture than did GM-CSF-derived BMDM and required only LPS stimulation to produce NO$\\sb2\\sp-$. In contrast, GM-CSF-derived BMDM secreted NO$\\sb2\\sp-$ only following treatment with IFN-$\\gamma$ plus LPS. When P815 tumor targets were used, GM-CSF-derived BMDM displayed higher basal and inducible levels of killing than CSF-1-derived BMDM and required only LPS treatment to reach full cytolytic capacity. Additionally, GM-CSF-derived BMDM showed greater listeriacidal capacity than did CSF-1-derived BMDM, particularly following IFN-$\\gamma$ plus LPS treatment. To assess immunocompetence under conditions resembling those of inflammatory sites, BMDM function was examined following treatment with PGE$\\sb2$ or in conditions of reduced L-arginine concentration. PGE$\\sb2$ (10$\\sp{-6}$-10$\\sp{-8}$ M) had no effect on BMDM ability to cytolyze L929 cells, kill intracellular Listeria, or produce NO$\\sb2\\sp-$, but GM-CSF-derived BMDM were inhibited 33% for cytolysis of K562 tumor cells. Interestingly, GM-CSF-derived BMDM were much less sensitive than CSF-1-derived BMDM for PGE$\\sb2$, but not cAMP-mediated inhibition of TNF-$\\alpha$. Arginine depletion blocked NO$\\sb2\\sp-$ production by both BMDM populations and the listeriacidal activity induced by IFN-$\\gamma$ plus LPS was abolished.","Macrophages were elicited in CB-17 and scid mice by repeated injection of GM-CSF. Following challenge with Listeria, scid mice which had been pretreated with GM-CSF showed reduced numbers of bacteria in the liver and spleens. CB-17 mice were unaffected by GM-CSF administration.","When used alone, neither CSF-1 nor GM-CSF elicited TNF-$\\alpha$, NO$\\sb2\\sp-$, or PGE$\\sb2$ secretion. GM-CSF primed CSF-1-derived BMDM for enhanced LPS-induced TNF-$\\alpha$, NO$\\sb2\\sp-$, and PGE$\\sb2$ secretion, and for augmented cytolysis of P815, but not K562 tumor cells. Thus, GM-CSF elicits a macrophage population with functional signal requirements distinct from those of CSF-1-derived BMDM and is a more effective biological response modifier for macrophage function than is CSF-1.","Made available in DSpace on 2011-05-07T12:35:11Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9124479.pdf: 5604868 bytes, checksum: f344b15fc1e4283f91fcce7c0589c192 (MD5) Previous issue date: 1991","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:42:56Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:18:44-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"]},{"key":"dc:title","label":"Title","values":["Differentiation and activation of functionally distinct macrophage populations by CSF-1 and GM-CSF"]}]}],"canonical_facts":{"dc:contributor":["Shapiro, Stuart Z."],"dc:creator":["Rutherford, Mark Stephen"],"dc:date":["2011-05-07T12:35:11Z","10000-01-01","1991"],"dc:description":["Macrophages derived in vitro from bone marrow progenitor cells (BMDM) under the influence of CSF-1 or GM-CSF were compared for immune function. CSF-1- and GM-CSF-derived BMDM did not differ in their ability to kill L929 tumor targets or produce IL-6 and LTC$\\sb4$ in response to IFN-$\\gamma$ and LPS. CSF-1-derived BMDM secreted more TNF-$\\alpha$ and PGE$\\sb2$ at early stages of culture than did GM-CSF-derived BMDM and required only LPS stimulation to produce NO$\\sb2\\sp-$. In contrast, GM-CSF-derived BMDM secreted NO$\\sb2\\sp-$ only following treatment with IFN-$\\gamma$ plus LPS. When P815 tumor targets were used, GM-CSF-derived BMDM displayed higher basal and inducible levels of killing than CSF-1-derived BMDM and required only LPS treatment to reach full cytolytic capacity. Additionally, GM-CSF-derived BMDM showed greater listeriacidal capacity than did CSF-1-derived BMDM, particularly following IFN-$\\gamma$ plus LPS treatment. To assess immunocompetence under conditions resembling those of inflammatory sites, BMDM function was examined following treatment with PGE$\\sb2$ or in conditions of reduced L-arginine concentration. PGE$\\sb2$ (10$\\sp{-6}$-10$\\sp{-8}$ M) had no effect on BMDM ability to cytolyze L929 cells, kill intracellular Listeria, or produce NO$\\sb2\\sp-$, but GM-CSF-derived BMDM were inhibited 33% for cytolysis of K562 tumor cells. Interestingly, GM-CSF-derived BMDM were much less sensitive than CSF-1-derived BMDM for PGE$\\sb2$, but not cAMP-mediated inhibition of TNF-$\\alpha$. Arginine depletion blocked NO$\\sb2\\sp-$ production by both BMDM populations and the listeriacidal activity induced by IFN-$\\gamma$ plus LPS was abolished.","Macrophages were elicited in CB-17 and scid mice by repeated injection of GM-CSF. Following challenge with Listeria, scid mice which had been pretreated with GM-CSF showed reduced numbers of bacteria in the liver and spleens. CB-17 mice were unaffected by GM-CSF administration.","When used alone, neither CSF-1 nor GM-CSF elicited TNF-$\\alpha$, NO$\\sb2\\sp-$, or PGE$\\sb2$ secretion. GM-CSF primed CSF-1-derived BMDM for enhanced LPS-induced TNF-$\\alpha$, NO$\\sb2\\sp-$, and PGE$\\sb2$ secretion, and for augmented cytolysis of P815, but not K562 tumor cells. Thus, GM-CSF elicits a macrophage population with functional signal requirements distinct from those of CSF-1-derived BMDM and is a more effective biological response modifier for macrophage function than is CSF-1.","Made available in DSpace on 2011-05-07T12:35:11Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9124479.pdf: 5604868 bytes, checksum: f344b15fc1e4283f91fcce7c0589c192 (MD5) Previous issue date: 1991","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:42:56Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:18:44-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"],"dc:identifier":["AAI9124479","(UMI)AAI9124479","http://hdl.handle.net/2142/20296"],"dc:language":["eng"],"dc:rights":["Copyright 1991 Rutherford, Mark Stephen"],"dc:subject":["Biology, Cell","Health Sciences, Immunology"],"dc:title":["Differentiation and activation of functionally distinct macrophage populations by CSF-1 and GM-CSF"],"dc:type":["text"],"thesis:degree_discipline":["Pathobiology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:25:15Z"}