Abatacept modulates proinflammatory macrophage responses upon cytokine-activated T cell and Toll-like receptor ligand stimulation
Objectives We investigated whether Abatacept might reduce proinflammatory cytokine production by macrophages upon contact with cytokine activated T cells and/or stimulation with TLR ligands. Methods Macrophages and cytokine stimulated T cells (Tck) were added together in the presence of Abatacept or...
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| Veröffentlicht in: | Annals of the rheumatic diseases 2012-01, Vol.71 (1), p.80-83 |
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| container_title | Annals of the rheumatic diseases |
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| creator | Wenink, M H Santegoets, K C M Platt, A M van den Berg, W B van Riel, P L C M Garside, P Radstake, T R D J McInnes, I B |
| description | Objectives We investigated whether Abatacept might reduce proinflammatory cytokine production by macrophages upon contact with cytokine activated T cells and/or stimulation with TLR ligands. Methods Macrophages and cytokine stimulated T cells (Tck) were added together in the presence of Abatacept or a control Ig, with or without TLR ligands. The production of cytokines was determined by luminex. Results Abatacept reduced Tck-induced production of TNFa by macrophages. Tck and TLR ligands synergistically induced the production of proinflammatory cytokines by macrophages, especially IL-12p70. The production of IL-12p70 coincided with the production of IFNg, which were both reduced in the presence of Abatacept. Conclusions Tck induce the production of TNFa by macrophages and facilitate the highly increased production of proinflammatory cytokines in the presence of TLR ligands. Abatacept was shown to potently suppress these pathways suggesting that its role may extend beyond antigen specific T cell mediated effector function. |
| doi_str_mv | 10.1136/annrheumdis-2011-200348 |
| format | Article |
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Methods Macrophages and cytokine stimulated T cells (Tck) were added together in the presence of Abatacept or a control Ig, with or without TLR ligands. The production of cytokines was determined by luminex. Results Abatacept reduced Tck-induced production of TNFa by macrophages. Tck and TLR ligands synergistically induced the production of proinflammatory cytokines by macrophages, especially IL-12p70. The production of IL-12p70 coincided with the production of IFNg, which were both reduced in the presence of Abatacept. Conclusions Tck induce the production of TNFa by macrophages and facilitate the highly increased production of proinflammatory cytokines in the presence of TLR ligands. Abatacept was shown to potently suppress these pathways suggesting that its role may extend beyond antigen specific T cell mediated effector function.</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/annrheumdis-2011-200348</identifier><identifier>PMID: 21908454</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><subject>Abatacept ; Antigens ; Biological and medical sciences ; Cell Communication - immunology ; Cells, Cultured ; Coculture Techniques ; Cytokines ; Cytokines - biosynthesis ; Cytokines - immunology ; Diseases of the osteoarticular system ; Drug Evaluation, Preclinical - methods ; Granulocytes ; Humans ; Immunoconjugates - pharmacology ; Immunomodulators ; Immunosuppressive Agents - pharmacology ; Inflammation Mediators - metabolism ; Interleukin-12 - biosynthesis ; Ligands ; Lymphocyte Activation - immunology ; Lymphocytes ; Macrophages - drug effects ; Macrophages - immunology ; Medical sciences ; Pharmacology. Drug treatments ; Proteins ; T cell receptors ; T-Lymphocytes - immunology ; Toll-Like Receptors - immunology ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - biosynthesis</subject><ispartof>Annals of the rheumatic diseases, 2012-01, Vol.71 (1), p.80-83</ispartof><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><rights>2015 INIST-CNRS</rights><rights>Copyright: 2011 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b553t-b51573ac622dd28a0f5cda5d37caebc60a819b5953429652aaa6cc99ed54e48e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://ard.bmj.com/content/71/1/80.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://ard.bmj.com/content/71/1/80.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,780,784,3196,23571,27924,27925,77600,77631</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25292885$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21908454$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wenink, M H</creatorcontrib><creatorcontrib>Santegoets, K C M</creatorcontrib><creatorcontrib>Platt, A M</creatorcontrib><creatorcontrib>van den Berg, W B</creatorcontrib><creatorcontrib>van Riel, P L C M</creatorcontrib><creatorcontrib>Garside, P</creatorcontrib><creatorcontrib>Radstake, T R D J</creatorcontrib><creatorcontrib>McInnes, I B</creatorcontrib><title>Abatacept modulates proinflammatory macrophage responses upon cytokine-activated T cell and Toll-like receptor ligand stimulation</title><title>Annals of the rheumatic diseases</title><addtitle>Ann Rheum Dis</addtitle><description>Objectives We investigated whether Abatacept might reduce proinflammatory cytokine production by macrophages upon contact with cytokine activated T cells and/or stimulation with TLR ligands. Methods Macrophages and cytokine stimulated T cells (Tck) were added together in the presence of Abatacept or a control Ig, with or without TLR ligands. The production of cytokines was determined by luminex. Results Abatacept reduced Tck-induced production of TNFa by macrophages. Tck and TLR ligands synergistically induced the production of proinflammatory cytokines by macrophages, especially IL-12p70. The production of IL-12p70 coincided with the production of IFNg, which were both reduced in the presence of Abatacept. Conclusions Tck induce the production of TNFa by macrophages and facilitate the highly increased production of proinflammatory cytokines in the presence of TLR ligands. Abatacept was shown to potently suppress these pathways suggesting that its role may extend beyond antigen specific T cell mediated effector function.</description><subject>Abatacept</subject><subject>Antigens</subject><subject>Biological and medical sciences</subject><subject>Cell Communication - immunology</subject><subject>Cells, Cultured</subject><subject>Coculture Techniques</subject><subject>Cytokines</subject><subject>Cytokines - biosynthesis</subject><subject>Cytokines - immunology</subject><subject>Diseases of the osteoarticular system</subject><subject>Drug Evaluation, Preclinical - methods</subject><subject>Granulocytes</subject><subject>Humans</subject><subject>Immunoconjugates - pharmacology</subject><subject>Immunomodulators</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin-12 - biosynthesis</subject><subject>Ligands</subject><subject>Lymphocyte Activation - immunology</subject><subject>Lymphocytes</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - immunology</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Proteins</subject><subject>T cell receptors</subject><subject>T-Lymphocytes - immunology</subject><subject>Toll-Like Receptors - immunology</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkcGO0zAQhiMEYsvCK0AkhDgFbCdO7OOqYlnEqnAoXK2J4-y6je1iJ4geeXMmSqkQF7h4PPb3z4z9Z9kLSt5QWtZvwft4bybX2VQwQikupKzEg2xFq1pgVpOH2YrgYVHJurnInqS0w5QIKh5nF4xKIiperbKfVy2MoM1hzF3opgFGk_JDDNb3AzgHY4jH3IGO4XAPdyaPJh2CTwhNGHN9HMPeelOAHu13FHf5NtdmGHLwuA3DUAx2P8vmFiHmg72bb9Jo3dzMBv80e9TDkMyzU7zMvly_265vittP7z-sr26LlvNyxJXypgRdM9Z1TADpue6Ad2WjwbS6JiCobLnkZcVkzRkA1FpLaTpemUqY8jJ7vdTF132bTBqVs2keFbwJU1KSCvw1SeS_SSIIkVwyJF_-Re7CFD0-Q9GmwXolkQKpZqHwF1OKpleHaB3Eo6JEzXaqP-xUs51qsROVz0_1p9aZ7qz77R8Cr04AJA1DH8FrrHHmOJNMCI5csXA2jebH-R7iXtVN2XC1-bpWn6vt9eYj3agb5NnCt27339P-AjUrzh0</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Wenink, M H</creator><creator>Santegoets, K C M</creator><creator>Platt, A M</creator><creator>van den Berg, W B</creator><creator>van Riel, P L C M</creator><creator>Garside, P</creator><creator>Radstake, T R D J</creator><creator>McInnes, I B</creator><general>BMJ Publishing Group Ltd and European League Against Rheumatism</general><general>BMJ Publishing Group</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20120101</creationdate><title>Abatacept modulates proinflammatory macrophage responses upon cytokine-activated T cell and Toll-like receptor ligand stimulation</title><author>Wenink, M H ; Santegoets, K C M ; Platt, A M ; van den Berg, W B ; van Riel, P L C M ; Garside, P ; Radstake, T R D J ; McInnes, I B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b553t-b51573ac622dd28a0f5cda5d37caebc60a819b5953429652aaa6cc99ed54e48e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Abatacept</topic><topic>Antigens</topic><topic>Biological and medical sciences</topic><topic>Cell Communication - immunology</topic><topic>Cells, Cultured</topic><topic>Coculture Techniques</topic><topic>Cytokines</topic><topic>Cytokines - biosynthesis</topic><topic>Cytokines - immunology</topic><topic>Diseases of the osteoarticular system</topic><topic>Drug Evaluation, Preclinical - methods</topic><topic>Granulocytes</topic><topic>Humans</topic><topic>Immunoconjugates - pharmacology</topic><topic>Immunomodulators</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin-12 - biosynthesis</topic><topic>Ligands</topic><topic>Lymphocyte Activation - immunology</topic><topic>Lymphocytes</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - immunology</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Proteins</topic><topic>T cell receptors</topic><topic>T-Lymphocytes - immunology</topic><topic>Toll-Like Receptors - immunology</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wenink, M H</creatorcontrib><creatorcontrib>Santegoets, K C M</creatorcontrib><creatorcontrib>Platt, A M</creatorcontrib><creatorcontrib>van den Berg, W B</creatorcontrib><creatorcontrib>van Riel, P L C M</creatorcontrib><creatorcontrib>Garside, P</creatorcontrib><creatorcontrib>Radstake, T R D J</creatorcontrib><creatorcontrib>McInnes, I B</creatorcontrib><collection>Istex</collection><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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Annals of the rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wenink, M H</au><au>Santegoets, K C M</au><au>Platt, A M</au><au>van den Berg, W B</au><au>van Riel, P L C M</au><au>Garside, P</au><au>Radstake, T R D J</au><au>McInnes, I B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Abatacept modulates proinflammatory macrophage responses upon cytokine-activated T cell and Toll-like receptor ligand stimulation</atitle><jtitle>Annals of the rheumatic diseases</jtitle><addtitle>Ann Rheum Dis</addtitle><date>2012-01-01</date><risdate>2012</risdate><volume>71</volume><issue>1</issue><spage>80</spage><epage>83</epage><pages>80-83</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><coden>ARDIAO</coden><abstract>Objectives We investigated whether Abatacept might reduce proinflammatory cytokine production by macrophages upon contact with cytokine activated T cells and/or stimulation with TLR ligands. Methods Macrophages and cytokine stimulated T cells (Tck) were added together in the presence of Abatacept or a control Ig, with or without TLR ligands. The production of cytokines was determined by luminex. Results Abatacept reduced Tck-induced production of TNFa by macrophages. Tck and TLR ligands synergistically induced the production of proinflammatory cytokines by macrophages, especially IL-12p70. The production of IL-12p70 coincided with the production of IFNg, which were both reduced in the presence of Abatacept. Conclusions Tck induce the production of TNFa by macrophages and facilitate the highly increased production of proinflammatory cytokines in the presence of TLR ligands. Abatacept was shown to potently suppress these pathways suggesting that its role may extend beyond antigen specific T cell mediated effector function.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and European League Against Rheumatism</pub><pmid>21908454</pmid><doi>10.1136/annrheumdis-2011-200348</doi><tpages>4</tpages></addata></record> |
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| subjects | Abatacept Antigens Biological and medical sciences Cell Communication - immunology Cells, Cultured Coculture Techniques Cytokines Cytokines - biosynthesis Cytokines - immunology Diseases of the osteoarticular system Drug Evaluation, Preclinical - methods Granulocytes Humans Immunoconjugates - pharmacology Immunomodulators Immunosuppressive Agents - pharmacology Inflammation Mediators - metabolism Interleukin-12 - biosynthesis Ligands Lymphocyte Activation - immunology Lymphocytes Macrophages - drug effects Macrophages - immunology Medical sciences Pharmacology. Drug treatments Proteins T cell receptors T-Lymphocytes - immunology Toll-Like Receptors - immunology Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - biosynthesis |
| title | Abatacept modulates proinflammatory macrophage responses upon cytokine-activated T cell and Toll-like receptor ligand stimulation |
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