Effects of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), IL‐2, interferon‐gamma (IFN‐γ), tumour necrosis factor‐alpha (TNF‐α) and IL‐6 on the production of immunoreactive IL‐1 and TNF‐α by human monocytes
SUMMARY The effects of GM‐CSF, IL‐2, IFN‐γ, TNF‐α and IL‐6 on the production of IL‐1 (both secreted and cell associated) and TNF‐α by peripheral blood monocytes were studied. Monocytes were cultured for 20 h in suspension and in serum‐free conditions which minimized background stimulation of monokin...
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| Veröffentlicht in: | Clinical and experimental immunology 1991-07, Vol.85 (1), p.143-150 |
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| creator | DANIS, V. A. FRANIC, G. M. RATHJEN, D. A. BROOKS, P. M. |
| description | SUMMARY
The effects of GM‐CSF, IL‐2, IFN‐γ, TNF‐α and IL‐6 on the production of IL‐1 (both secreted and cell associated) and TNF‐α by peripheral blood monocytes were studied. Monocytes were cultured for 20 h in suspension and in serum‐free conditions which minimized background stimulation of monokine production. GM‐CSF, IL‐2 and TNF‐α directly induced the production of cell‐associated IL‐1 but little or no IL‐1 or TNF‐α secretion. Combination of GM‐CSF with IFN‐γ, IL‐2 or TNF‐α synergistically enhanced IL‐1 secretion and had an additive effect on cell‐associated IL‐1 production. Combination of IL‐2 with IFN‐γ or TNF‐α also synergistically enhanced IL‐1 secretion but the effect on cell‐associated IL‐1 production was less than additive. GM‐CSF synergisticaily enhanced TNF‐α secretion induced by IFN‐γ but not by tipopolysaccharide. GM‐CSF did not enhance TNF‐α secretion induced by IL‐2 or TNF‐α. In contrast, IL‐2 synergistically enhanced TNF‐α secretion induced by IFN‐γ. These results are discussed in relation to cytokine involvement in rheumatoid arthritis. |
| doi_str_mv | 10.1111/j.1365-2249.1991.tb05695.x |
| format | Article |
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The effects of GM‐CSF, IL‐2, IFN‐γ, TNF‐α and IL‐6 on the production of IL‐1 (both secreted and cell associated) and TNF‐α by peripheral blood monocytes were studied. Monocytes were cultured for 20 h in suspension and in serum‐free conditions which minimized background stimulation of monokine production. GM‐CSF, IL‐2 and TNF‐α directly induced the production of cell‐associated IL‐1 but little or no IL‐1 or TNF‐α secretion. Combination of GM‐CSF with IFN‐γ, IL‐2 or TNF‐α synergistically enhanced IL‐1 secretion and had an additive effect on cell‐associated IL‐1 production. Combination of IL‐2 with IFN‐γ or TNF‐α also synergistically enhanced IL‐1 secretion but the effect on cell‐associated IL‐1 production was less than additive. GM‐CSF synergisticaily enhanced TNF‐α secretion induced by IFN‐γ but not by tipopolysaccharide. GM‐CSF did not enhance TNF‐α secretion induced by IL‐2 or TNF‐α. In contrast, IL‐2 synergistically enhanced TNF‐α secretion induced by IFN‐γ. These results are discussed in relation to cytokine involvement in rheumatoid arthritis.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/j.1365-2249.1991.tb05695.x</identifier><identifier>PMID: 1906383</identifier><identifier>CODEN: CEXIAL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Analysis of the immune response. Humoral and cellular immunity ; Biological and medical sciences ; Cells, Cultured ; colony‐stimulating factor interleukin‐2 ; Cytokines - pharmacology ; Dose-Response Relationship, Drug ; Drug Combinations ; Drug Synergism ; Enzyme-Linked Immunosorbent Assay ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology ; Humans ; Immunobiology ; Interferon-gamma - pharmacology ; Interleukin-1 - biosynthesis ; Interleukin-2 - pharmacology ; Interleukin-6 - pharmacology ; interleukin‐1 ; Lipopolysaccharides - pharmacology ; Miscellaneous ; monocytes ; Monocytes - drug effects ; Monocytes - metabolism ; Recombinant Proteins - pharmacology ; Regulatory factors and their cellular receptors ; Tumor Necrosis Factor-alpha - biosynthesis ; Tumor Necrosis Factor-alpha - pharmacology ; tumour necrosis factor</subject><ispartof>Clinical and experimental immunology, 1991-07, Vol.85 (1), p.143-150</ispartof><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5063-e84834080461f954e2693f12ed5e0fa442207cab3f86cc3c92fc6eb00091e5403</citedby><cites>FETCH-LOGICAL-c5063-e84834080461f954e2693f12ed5e0fa442207cab3f86cc3c92fc6eb00091e5403</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1535710/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1535710/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19833913$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1906383$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DANIS, V. A.</creatorcontrib><creatorcontrib>FRANIC, G. M.</creatorcontrib><creatorcontrib>RATHJEN, D. A.</creatorcontrib><creatorcontrib>BROOKS, P. M.</creatorcontrib><title>Effects of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), IL‐2, interferon‐gamma (IFN‐γ), tumour necrosis factor‐alpha (TNF‐α) and IL‐6 on the production of immunoreactive IL‐1 and TNF‐α by human monocytes</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>SUMMARY
The effects of GM‐CSF, IL‐2, IFN‐γ, TNF‐α and IL‐6 on the production of IL‐1 (both secreted and cell associated) and TNF‐α by peripheral blood monocytes were studied. Monocytes were cultured for 20 h in suspension and in serum‐free conditions which minimized background stimulation of monokine production. GM‐CSF, IL‐2 and TNF‐α directly induced the production of cell‐associated IL‐1 but little or no IL‐1 or TNF‐α secretion. Combination of GM‐CSF with IFN‐γ, IL‐2 or TNF‐α synergistically enhanced IL‐1 secretion and had an additive effect on cell‐associated IL‐1 production. Combination of IL‐2 with IFN‐γ or TNF‐α also synergistically enhanced IL‐1 secretion but the effect on cell‐associated IL‐1 production was less than additive. GM‐CSF synergisticaily enhanced TNF‐α secretion induced by IFN‐γ but not by tipopolysaccharide. GM‐CSF did not enhance TNF‐α secretion induced by IL‐2 or TNF‐α. In contrast, IL‐2 synergistically enhanced TNF‐α secretion induced by IFN‐γ. These results are discussed in relation to cytokine involvement in rheumatoid arthritis.</description><subject>Analysis of the immune response. Humoral and cellular immunity</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>colony‐stimulating factor interleukin‐2</subject><subject>Cytokines - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Combinations</subject><subject>Drug Synergism</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</subject><subject>Humans</subject><subject>Immunobiology</subject><subject>Interferon-gamma - pharmacology</subject><subject>Interleukin-1 - biosynthesis</subject><subject>Interleukin-2 - pharmacology</subject><subject>Interleukin-6 - pharmacology</subject><subject>interleukin‐1</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Miscellaneous</subject><subject>monocytes</subject><subject>Monocytes - drug effects</subject><subject>Monocytes - metabolism</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Regulatory factors and their cellular receptors</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>tumour necrosis factor</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVUk1uEzEYHSFQCYUjIFlISKnUBHvsceMukFCUlEihLChry3HsiaOxHdme0uw4AldB3INDcAROgKcT2rLEG_vze9_7foviFYJjlM-b7RhhWo3KkrAxYgyN0wpWlFXjm0fF4A56XAwghGzEECRPi2cxbrNJKS2PiiPEIMUTPCh-z7RWMkXgNaiDcG3j5T6pX1-_WSGD321ErYD0jXf7_BeTsW0jknE10EImH8Dw4kMGpp_mJ6dgsczP8hQYl1TQKniX7VpYK8BwMb_Mxs8fmZZa69sAnMoBookHpYyKJscDw6vLeUf9fgKEW_eiFHgH0kaBXfDrViaTzZyxsbZ1PqgsYK5VT0W3Xn81wGoPNq0VDljvbkuLz4snWjRRvTjcx8Xn-exq-n60_HixmL5bjmSVmzNSEzLBBE4goUiziqiSMqxRqdaVgloQUpbwTIoV1hMqJZas1JKqVddypCoC8XHxttfdtSur1lK5FETDd8FYEfbcC8P_RZzZ8Npfc1Th6gx1Aue9QNenGJS-80WQd4vAt7ybNu-mzbtF4IdF4DfZ-eXD6Peu_eQz_vqAiyhFo_PspYkPaJnDEL6v4otp1P4_MuDT2QIRjP8AV-7gQQ</recordid><startdate>199107</startdate><enddate>199107</enddate><creator>DANIS, V. A.</creator><creator>FRANIC, G. M.</creator><creator>RATHJEN, D. A.</creator><creator>BROOKS, P. M.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>199107</creationdate><title>Effects of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), IL‐2, interferon‐gamma (IFN‐γ), tumour necrosis factor‐alpha (TNF‐α) and IL‐6 on the production of immunoreactive IL‐1 and TNF‐α by human monocytes</title><author>DANIS, V. A. ; FRANIC, G. M. ; RATHJEN, D. A. ; BROOKS, P. M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5063-e84834080461f954e2693f12ed5e0fa442207cab3f86cc3c92fc6eb00091e5403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Analysis of the immune response. Humoral and cellular immunity</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>colony‐stimulating factor interleukin‐2</topic><topic>Cytokines - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Combinations</topic><topic>Drug Synergism</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology</topic><topic>Humans</topic><topic>Immunobiology</topic><topic>Interferon-gamma - pharmacology</topic><topic>Interleukin-1 - biosynthesis</topic><topic>Interleukin-2 - pharmacology</topic><topic>Interleukin-6 - pharmacology</topic><topic>interleukin‐1</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Miscellaneous</topic><topic>monocytes</topic><topic>Monocytes - drug effects</topic><topic>Monocytes - metabolism</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Regulatory factors and their cellular receptors</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>tumour necrosis factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DANIS, V. A.</creatorcontrib><creatorcontrib>FRANIC, G. M.</creatorcontrib><creatorcontrib>RATHJEN, D. A.</creatorcontrib><creatorcontrib>BROOKS, P. M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DANIS, V. A.</au><au>FRANIC, G. M.</au><au>RATHJEN, D. A.</au><au>BROOKS, P. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), IL‐2, interferon‐gamma (IFN‐γ), tumour necrosis factor‐alpha (TNF‐α) and IL‐6 on the production of immunoreactive IL‐1 and TNF‐α by human monocytes</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>1991-07</date><risdate>1991</risdate><volume>85</volume><issue>1</issue><spage>143</spage><epage>150</epage><pages>143-150</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><coden>CEXIAL</coden><abstract>SUMMARY
The effects of GM‐CSF, IL‐2, IFN‐γ, TNF‐α and IL‐6 on the production of IL‐1 (both secreted and cell associated) and TNF‐α by peripheral blood monocytes were studied. Monocytes were cultured for 20 h in suspension and in serum‐free conditions which minimized background stimulation of monokine production. GM‐CSF, IL‐2 and TNF‐α directly induced the production of cell‐associated IL‐1 but little or no IL‐1 or TNF‐α secretion. Combination of GM‐CSF with IFN‐γ, IL‐2 or TNF‐α synergistically enhanced IL‐1 secretion and had an additive effect on cell‐associated IL‐1 production. Combination of IL‐2 with IFN‐γ or TNF‐α also synergistically enhanced IL‐1 secretion but the effect on cell‐associated IL‐1 production was less than additive. GM‐CSF synergisticaily enhanced TNF‐α secretion induced by IFN‐γ but not by tipopolysaccharide. GM‐CSF did not enhance TNF‐α secretion induced by IL‐2 or TNF‐α. In contrast, IL‐2 synergistically enhanced TNF‐α secretion induced by IFN‐γ. These results are discussed in relation to cytokine involvement in rheumatoid arthritis.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>1906383</pmid><doi>10.1111/j.1365-2249.1991.tb05695.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0009-9104 |
| ispartof | Clinical and experimental immunology, 1991-07, Vol.85 (1), p.143-150 |
| issn | 0009-9104 1365-2249 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1535710 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Analysis of the immune response. Humoral and cellular immunity Biological and medical sciences Cells, Cultured colony‐stimulating factor interleukin‐2 Cytokines - pharmacology Dose-Response Relationship, Drug Drug Combinations Drug Synergism Enzyme-Linked Immunosorbent Assay Fundamental and applied biological sciences. Psychology Fundamental immunology Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology Humans Immunobiology Interferon-gamma - pharmacology Interleukin-1 - biosynthesis Interleukin-2 - pharmacology Interleukin-6 - pharmacology interleukin‐1 Lipopolysaccharides - pharmacology Miscellaneous monocytes Monocytes - drug effects Monocytes - metabolism Recombinant Proteins - pharmacology Regulatory factors and their cellular receptors Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - pharmacology tumour necrosis factor |
| title | Effects of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), IL‐2, interferon‐gamma (IFN‐γ), tumour necrosis factor‐alpha (TNF‐α) and IL‐6 on the production of immunoreactive IL‐1 and TNF‐α by human monocytes |
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