OP0058 CCR6+ T-cells in children with juvenile idiopathic arthritis

OP0058 CCR6+ T-cells in children with juvenile idiopathic arthritis

Background Previous studies have demonstrated a plasticity of effector-T-cells regarding CCR6 expression in autoimmune disorders. In healthy humans, CCR6+ T-cells have been shown to belong mainly to the Th17 phenotype (characterized by IL-17 production) and CCR6- T-cells to the Th1 phenotype (IFNγ p...

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Veröffentlicht in:Annals of the rheumatic diseases 2013-06, Vol.71 (Suppl 3), p.72-72
Hauptverfasser: Sustal, K.N., Almanzar, G., Trippen, R., Höfner, K., Prelog, M.
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container_issue Suppl 3
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container_title Annals of the rheumatic diseases
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creator Sustal, K.N.
Almanzar, G.
Trippen, R.
Höfner, K.
Prelog, M.
description Background Previous studies have demonstrated a plasticity of effector-T-cells regarding CCR6 expression in autoimmune disorders. In healthy humans, CCR6+ T-cells have been shown to belong mainly to the Th17 phenotype (characterized by IL-17 production) and CCR6- T-cells to the Th1 phenotype (IFNγ production). Objectives The present study was aimed to investigate the CCR6+ T-cell phenotype and its plasticity in children with Juvenile idiopathic arthritis (JIA). Methods Peripheral blood mononuclear cells (PBMCs) of children with JIA (n=25 in clinical remission on medication; n=10 with disease flare) and age-matched healthy donors (HD) (n=21) were analyzed by flowcytometry to assess the phenotype, cytokine production and proliferation of T-cells expressing the chemokine receptor CCR6+. CCR6+ T-cells were separated via magnetic bead isolation. Results The proportion of CCR6+ T-cells (CD4+ gate) was significantly increased in patients with disease flare (mean 6.3±3.7%) compared to those in remission (3.3±2.7%) or HD (4.0±1.9%) (p
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In healthy humans, CCR6+ T-cells have been shown to belong mainly to the Th17 phenotype (characterized by IL-17 production) and CCR6- T-cells to the Th1 phenotype (IFNγ production). Objectives The present study was aimed to investigate the CCR6+ T-cell phenotype and its plasticity in children with Juvenile idiopathic arthritis (JIA). Methods Peripheral blood mononuclear cells (PBMCs) of children with JIA (n=25 in clinical remission on medication; n=10 with disease flare) and age-matched healthy donors (HD) (n=21) were analyzed by flowcytometry to assess the phenotype, cytokine production and proliferation of T-cells expressing the chemokine receptor CCR6+. CCR6+ T-cells were separated via magnetic bead isolation. Results The proportion of CCR6+ T-cells (CD4+ gate) was significantly increased in patients with disease flare (mean 6.3±3.7%) compared to those in remission (3.3±2.7%) or HD (4.0±1.9%) (p&lt;0.05). Regarding the phenotype, almost all CCR6+ T-cells expressed RORgt and CD45RO, but some were CCR7- (77%). Additionally, in JIA patients in remission, about 12.5% of CCR6+ T-cells showed CD161 expression, a marker for the concomitant Th1/Th17 phenotype found in some cases of adult arthritis. CCR6- T-cells were mainly CD45RA+ (50%) and CCR7+ (51.3%), but lost CD161 expression (2.2%). Separated CCR6+ T-cells of JIA patients showed a 17.7-fold higher IL-17 production compared to CCR6- T-cells. However, no significant difference in IFNγ production was determined between CCR6+ or CCR6- T-cell subsets. Conclusions Our preliminary results confirmed that the CCR6+ T-cell-pool mainly represents the IL-17-producing T-cell subset in JIA patients with disease flare, as well as in remission. Whether CCR6+ T-cells in JIA patients appear to be stable under various cytokine milieus or treatments with biologicals and, thus, offer to be a promising target for future therapies has to be investigated. Disclosure of Interest None Declared</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/annrheumdis-2012-eular.1741</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><ispartof>Annals of the rheumatic diseases, 2013-06, Vol.71 (Suppl 3), p.72-72</ispartof><rights>2013, 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>Copyright: 2013 (c) 2013, 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></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://ard.bmj.com/content/71/Suppl_3/72.3.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://ard.bmj.com/content/71/Suppl_3/72.3.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,315,782,786,3200,23580,27933,27934,77610,77641</link.rule.ids></links><search><creatorcontrib>Sustal, K.N.</creatorcontrib><creatorcontrib>Almanzar, G.</creatorcontrib><creatorcontrib>Trippen, R.</creatorcontrib><creatorcontrib>Höfner, K.</creatorcontrib><creatorcontrib>Prelog, M.</creatorcontrib><title>OP0058 CCR6+ T-cells in children with juvenile idiopathic arthritis</title><title>Annals of the rheumatic diseases</title><addtitle>Ann Rheum Dis</addtitle><description>Background Previous studies have demonstrated a plasticity of effector-T-cells regarding CCR6 expression in autoimmune disorders. In healthy humans, CCR6+ T-cells have been shown to belong mainly to the Th17 phenotype (characterized by IL-17 production) and CCR6- T-cells to the Th1 phenotype (IFNγ production). Objectives The present study was aimed to investigate the CCR6+ T-cell phenotype and its plasticity in children with Juvenile idiopathic arthritis (JIA). Methods Peripheral blood mononuclear cells (PBMCs) of children with JIA (n=25 in clinical remission on medication; n=10 with disease flare) and age-matched healthy donors (HD) (n=21) were analyzed by flowcytometry to assess the phenotype, cytokine production and proliferation of T-cells expressing the chemokine receptor CCR6+. CCR6+ T-cells were separated via magnetic bead isolation. Results The proportion of CCR6+ T-cells (CD4+ gate) was significantly increased in patients with disease flare (mean 6.3±3.7%) compared to those in remission (3.3±2.7%) or HD (4.0±1.9%) (p&lt;0.05). Regarding the phenotype, almost all CCR6+ T-cells expressed RORgt and CD45RO, but some were CCR7- (77%). Additionally, in JIA patients in remission, about 12.5% of CCR6+ T-cells showed CD161 expression, a marker for the concomitant Th1/Th17 phenotype found in some cases of adult arthritis. CCR6- T-cells were mainly CD45RA+ (50%) and CCR7+ (51.3%), but lost CD161 expression (2.2%). Separated CCR6+ T-cells of JIA patients showed a 17.7-fold higher IL-17 production compared to CCR6- T-cells. However, no significant difference in IFNγ production was determined between CCR6+ or CCR6- T-cell subsets. Conclusions Our preliminary results confirmed that the CCR6+ T-cell-pool mainly represents the IL-17-producing T-cell subset in JIA patients with disease flare, as well as in remission. Whether CCR6+ T-cells in JIA patients appear to be stable under various cytokine milieus or treatments with biologicals and, thus, offer to be a promising target for future therapies has to be investigated. Disclosure of Interest None Declared</description><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqVkMtOwzAQRS0EEqXwD5G6RC4eJ7EdsUJReYhCK1QeO8tJHMUlTYqd8Nix4Uf5ElKCEFtWoxmdO1c6CI2AjAF8dqSqyha6XWXGYUqAYt2Wyo6BB7CFBhAw0Z0Z2UYDQoiPg4jxXbTn3LJbiQAxQJPZnJBQfL5_xPENO_QWONVl6TxTeWlhyszqynsxTeEt22ddmVJ7JjP1WjWFST1lm8Kaxrh9tJOr0umDnzlEt6eTRXyOp7Ozi_hkihNgYYBTmkV5KpgQlNAsDCkXHHIahDoTKU848QULo4glmrAgV4mfAADxCWgIfSWYP0Sj_u_a1k-tdo1c1q2tukoJnPOIc8qCjjruqdTWzlmdy7U1K2XfJBC58Sb_eJMbb_Lbm9x469K4TxvX6NffqLKPknGfh_L6Lu5CV_c38-BSPnQ86_lktfxX0RfcfIZ_</recordid><startdate>201306</startdate><enddate>201306</enddate><creator>Sustal, K.N.</creator><creator>Almanzar, G.</creator><creator>Trippen, R.</creator><creator>Höfner, K.</creator><creator>Prelog, M.</creator><general>BMJ Publishing Group Ltd and European League Against Rheumatism</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</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></search><sort><creationdate>201306</creationdate><title>OP0058 CCR6+ T-cells in children with juvenile idiopathic arthritis</title><author>Sustal, K.N. ; Almanzar, G. ; Trippen, R. ; Höfner, K. ; Prelog, M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b1654-c2d9fc8688202d5527871f245ed8c7b703865996be064fab3b1110301e153a863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sustal, K.N.</creatorcontrib><creatorcontrib>Almanzar, G.</creatorcontrib><creatorcontrib>Trippen, R.</creatorcontrib><creatorcontrib>Höfner, K.</creatorcontrib><creatorcontrib>Prelog, M.</creatorcontrib><collection>Istex</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health &amp; 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 &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health &amp; 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><jtitle>Annals of the rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sustal, K.N.</au><au>Almanzar, G.</au><au>Trippen, R.</au><au>Höfner, K.</au><au>Prelog, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>OP0058 CCR6+ T-cells in children with juvenile idiopathic arthritis</atitle><jtitle>Annals of the rheumatic diseases</jtitle><addtitle>Ann Rheum Dis</addtitle><date>2013-06</date><risdate>2013</risdate><volume>71</volume><issue>Suppl 3</issue><spage>72</spage><epage>72</epage><pages>72-72</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><coden>ARDIAO</coden><abstract>Background Previous studies have demonstrated a plasticity of effector-T-cells regarding CCR6 expression in autoimmune disorders. In healthy humans, CCR6+ T-cells have been shown to belong mainly to the Th17 phenotype (characterized by IL-17 production) and CCR6- T-cells to the Th1 phenotype (IFNγ production). Objectives The present study was aimed to investigate the CCR6+ T-cell phenotype and its plasticity in children with Juvenile idiopathic arthritis (JIA). Methods Peripheral blood mononuclear cells (PBMCs) of children with JIA (n=25 in clinical remission on medication; n=10 with disease flare) and age-matched healthy donors (HD) (n=21) were analyzed by flowcytometry to assess the phenotype, cytokine production and proliferation of T-cells expressing the chemokine receptor CCR6+. CCR6+ T-cells were separated via magnetic bead isolation. Results The proportion of CCR6+ T-cells (CD4+ gate) was significantly increased in patients with disease flare (mean 6.3±3.7%) compared to those in remission (3.3±2.7%) or HD (4.0±1.9%) (p&lt;0.05). Regarding the phenotype, almost all CCR6+ T-cells expressed RORgt and CD45RO, but some were CCR7- (77%). Additionally, in JIA patients in remission, about 12.5% of CCR6+ T-cells showed CD161 expression, a marker for the concomitant Th1/Th17 phenotype found in some cases of adult arthritis. CCR6- T-cells were mainly CD45RA+ (50%) and CCR7+ (51.3%), but lost CD161 expression (2.2%). Separated CCR6+ T-cells of JIA patients showed a 17.7-fold higher IL-17 production compared to CCR6- T-cells. However, no significant difference in IFNγ production was determined between CCR6+ or CCR6- T-cell subsets. Conclusions Our preliminary results confirmed that the CCR6+ T-cell-pool mainly represents the IL-17-producing T-cell subset in JIA patients with disease flare, as well as in remission. Whether CCR6+ T-cells in JIA patients appear to be stable under various cytokine milieus or treatments with biologicals and, thus, offer to be a promising target for future therapies has to be investigated. Disclosure of Interest None Declared</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and European League Against Rheumatism</pub><doi>10.1136/annrheumdis-2012-eular.1741</doi><tpages>1</tpages></addata></record>
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title OP0058 CCR6+ T-cells in children with juvenile idiopathic arthritis
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