Dopamine favors expansion of glucocorticoid-resistant IL-17-producing T cells in multiple sclerosis
Abstract Dopamine (DA) is a neurotransmitter produced mainly in the central nervous system (CNS) that has immunomodulatory actions on T cells. As the multiple sclerosis (MS) has long been regarded as an autoimmune disease of CNS mediated by T cells, the objective of this study was to evaluate the im...
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| creator | Ferreira, Thais B Barros, Priscila O Teixeira, Bruna Cassano, Tatiane Centurião, Newton Kasahara, Taissa M Hygino, Joana Vasconcelos, Claudia Cristina F Filho, Helcio Alvarenga Alvarenga, Regina Wing, Ana Cristina Andrade, Regis M Andrade, Arnaldo F Bento, Cleonice A.M |
| description | Abstract Dopamine (DA) is a neurotransmitter produced mainly in the central nervous system (CNS) that has immunomodulatory actions on T cells. As the multiple sclerosis (MS) has long been regarded as an autoimmune disease of CNS mediated by T cells, the objective of this study was to evaluate the impact of DA on in vitro functional status of T cells from relapsing–remitting (RR)–MS patients. Peripheral T-cells from RR–MS patients were activated by mitogens and cell proliferation and cytokine production were assayed by [3 H]-thymidine uptake and ELISA, respectively. Our results demonstrated that DA enhanced in vitro T cell proliferation and Th17-related cytokines in MS-derived cell cultures. In addition, this catecholamine reduced Treg-related cytokines (IL-10 and TGF-β) release by activated CD4+ T cells. These DA-induced effects on T cells were mainly dependent on IL-6 production by both polyclonally-activated CD4+ T cells and LPS-stimulated monocytes. Furthermore, the production of IL-17 and IL-6 by MS-derived T cells was directly related with neurological disability (EDSS score), and the release of these cytokines was less sensitive to glucocorticoid inhibition in MS patients than in control group, mainly after DA addition. In conclusion, our data suggest that DA amplifies glucocorticoid-resistant Th17 phenotype in MS patients, and this phenomenon could be, at least in part, due to its ability to induce IL-6 production by monocytes and CD4+ T cells. |
| doi_str_mv | 10.1016/j.bbi.2014.05.013 |
| format | Article |
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As the multiple sclerosis (MS) has long been regarded as an autoimmune disease of CNS mediated by T cells, the objective of this study was to evaluate the impact of DA on in vitro functional status of T cells from relapsing–remitting (RR)–MS patients. Peripheral T-cells from RR–MS patients were activated by mitogens and cell proliferation and cytokine production were assayed by [3 H]-thymidine uptake and ELISA, respectively. Our results demonstrated that DA enhanced in vitro T cell proliferation and Th17-related cytokines in MS-derived cell cultures. In addition, this catecholamine reduced Treg-related cytokines (IL-10 and TGF-β) release by activated CD4+ T cells. These DA-induced effects on T cells were mainly dependent on IL-6 production by both polyclonally-activated CD4+ T cells and LPS-stimulated monocytes. Furthermore, the production of IL-17 and IL-6 by MS-derived T cells was directly related with neurological disability (EDSS score), and the release of these cytokines was less sensitive to glucocorticoid inhibition in MS patients than in control group, mainly after DA addition. In conclusion, our data suggest that DA amplifies glucocorticoid-resistant Th17 phenotype in MS patients, and this phenomenon could be, at least in part, due to its ability to induce IL-6 production by monocytes and CD4+ T cells.</description><identifier>ISSN: 0889-1591</identifier><identifier>EISSN: 1090-2139</identifier><identifier>DOI: 10.1016/j.bbi.2014.05.013</identifier><identifier>PMID: 24882215</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Adult ; Allergy and Immunology ; CD4-Positive T-Lymphocytes - drug effects ; CD4-Positive T-Lymphocytes - metabolism ; Cell Division ; Cells, Cultured ; Cytokines ; Dopamine ; Dopamine - pharmacology ; Drug Resistance ; Female ; Humans ; IL-10 ; Interleukin-10 - biosynthesis ; Interleukin-10 - genetics ; Interleukin-6 - biosynthesis ; Interleukin-6 - genetics ; Lipopolysaccharide ; Lymphocyte Activation ; Male ; Middle Aged ; Monocytes - drug effects ; Monocytes - metabolism ; Multiple sclerosis ; Multiple Sclerosis, Relapsing-Remitting - immunology ; Multiple Sclerosis, Relapsing-Remitting - metabolism ; Neuroimmunomodulation - physiology ; Phytohemagglutinins - pharmacology ; Psychiatry ; Severity of Illness Index ; T cells ; Th17 ; Th17 Cells - immunology ; Transforming Growth Factor beta - biosynthesis ; Transforming Growth Factor beta - genetics ; Young Adult</subject><ispartof>Brain, behavior, and immunity, 2014-10, Vol.41, p.182-190</ispartof><rights>Elsevier Inc.</rights><rights>2014 Elsevier Inc.</rights><rights>Copyright © 2014 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c511t-9d1da23260cec22435f71c60b5f1752816df07de5938cc70894070dd59b0ff7d3</citedby><cites>FETCH-LOGICAL-c511t-9d1da23260cec22435f71c60b5f1752816df07de5938cc70894070dd59b0ff7d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0889159114001354$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24882215$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ferreira, Thais B</creatorcontrib><creatorcontrib>Barros, Priscila O</creatorcontrib><creatorcontrib>Teixeira, Bruna</creatorcontrib><creatorcontrib>Cassano, Tatiane</creatorcontrib><creatorcontrib>Centurião, Newton</creatorcontrib><creatorcontrib>Kasahara, Taissa M</creatorcontrib><creatorcontrib>Hygino, Joana</creatorcontrib><creatorcontrib>Vasconcelos, Claudia Cristina F</creatorcontrib><creatorcontrib>Filho, Helcio Alvarenga</creatorcontrib><creatorcontrib>Alvarenga, Regina</creatorcontrib><creatorcontrib>Wing, Ana Cristina</creatorcontrib><creatorcontrib>Andrade, Regis M</creatorcontrib><creatorcontrib>Andrade, Arnaldo F</creatorcontrib><creatorcontrib>Bento, Cleonice A.M</creatorcontrib><title>Dopamine favors expansion of glucocorticoid-resistant IL-17-producing T cells in multiple sclerosis</title><title>Brain, behavior, and immunity</title><addtitle>Brain Behav Immun</addtitle><description>Abstract Dopamine (DA) is a neurotransmitter produced mainly in the central nervous system (CNS) that has immunomodulatory actions on T cells. As the multiple sclerosis (MS) has long been regarded as an autoimmune disease of CNS mediated by T cells, the objective of this study was to evaluate the impact of DA on in vitro functional status of T cells from relapsing–remitting (RR)–MS patients. Peripheral T-cells from RR–MS patients were activated by mitogens and cell proliferation and cytokine production were assayed by [3 H]-thymidine uptake and ELISA, respectively. Our results demonstrated that DA enhanced in vitro T cell proliferation and Th17-related cytokines in MS-derived cell cultures. In addition, this catecholamine reduced Treg-related cytokines (IL-10 and TGF-β) release by activated CD4+ T cells. These DA-induced effects on T cells were mainly dependent on IL-6 production by both polyclonally-activated CD4+ T cells and LPS-stimulated monocytes. Furthermore, the production of IL-17 and IL-6 by MS-derived T cells was directly related with neurological disability (EDSS score), and the release of these cytokines was less sensitive to glucocorticoid inhibition in MS patients than in control group, mainly after DA addition. In conclusion, our data suggest that DA amplifies glucocorticoid-resistant Th17 phenotype in MS patients, and this phenomenon could be, at least in part, due to its ability to induce IL-6 production by monocytes and CD4+ T cells.</description><subject>Adult</subject><subject>Allergy and Immunology</subject><subject>CD4-Positive T-Lymphocytes - drug effects</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>Cell Division</subject><subject>Cells, Cultured</subject><subject>Cytokines</subject><subject>Dopamine</subject><subject>Dopamine - pharmacology</subject><subject>Drug Resistance</subject><subject>Female</subject><subject>Humans</subject><subject>IL-10</subject><subject>Interleukin-10 - biosynthesis</subject><subject>Interleukin-10 - genetics</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Interleukin-6 - genetics</subject><subject>Lipopolysaccharide</subject><subject>Lymphocyte Activation</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Monocytes - drug effects</subject><subject>Monocytes - metabolism</subject><subject>Multiple sclerosis</subject><subject>Multiple Sclerosis, Relapsing-Remitting - immunology</subject><subject>Multiple Sclerosis, Relapsing-Remitting - metabolism</subject><subject>Neuroimmunomodulation - physiology</subject><subject>Phytohemagglutinins - pharmacology</subject><subject>Psychiatry</subject><subject>Severity of Illness Index</subject><subject>T cells</subject><subject>Th17</subject><subject>Th17 Cells - immunology</subject><subject>Transforming Growth Factor beta - biosynthesis</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Young Adult</subject><issn>0889-1591</issn><issn>1090-2139</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkkuP1DAQhC0EYoeBH8AF-cgloduO8xASElpeK43EgeVsJXZn5SGxBztZ7f57HM3CgQOcfKmvul3VjL1EKBGwfnMsh8GVArAqQZWA8hHbIXRQCJTdY7aDtu0KVB1esGcpHQFASWyfsgtRta0QqHbMfAinfnae-Njfhpg43Z16n1zwPIz8ZlpNMCEuzgRni0jJpaX3C786FNgUpxjsapy_4dfc0DQl7jyf12lxp4l4MhPFkInn7MnYT4lePLx79v3Tx-vLL8Xh6-ery_eHwijEpegs2l5IUYMhI0Ql1digqWFQIzZKtFjbERpLqpOtMQ20XQUNWKu6AcaxsXLPXp99814_V0qLnl3a9uo9hTVprGXXtY1S-H-pqkVdS5ln7RmepSZ_JkUa9Sm6uY_3GkFvNeijzjXorQYNSucaMvPqwX4dZrJ_iN-5Z8Hbs4ByHreOok7GkTdkXSSzaBvcP-3f_UWbyXln-ukH3VM6hjX6HLRGnYQG_W27g-0MsIKMq0r-AjQhrIc</recordid><startdate>20141001</startdate><enddate>20141001</enddate><creator>Ferreira, Thais B</creator><creator>Barros, Priscila O</creator><creator>Teixeira, Bruna</creator><creator>Cassano, Tatiane</creator><creator>Centurião, Newton</creator><creator>Kasahara, Taissa M</creator><creator>Hygino, Joana</creator><creator>Vasconcelos, Claudia Cristina F</creator><creator>Filho, Helcio Alvarenga</creator><creator>Alvarenga, Regina</creator><creator>Wing, Ana Cristina</creator><creator>Andrade, Regis M</creator><creator>Andrade, Arnaldo F</creator><creator>Bento, Cleonice A.M</creator><general>Elsevier Inc</general><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>7X8</scope><scope>7QG</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope></search><sort><creationdate>20141001</creationdate><title>Dopamine favors expansion of glucocorticoid-resistant IL-17-producing T cells in multiple sclerosis</title><author>Ferreira, Thais B ; 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As the multiple sclerosis (MS) has long been regarded as an autoimmune disease of CNS mediated by T cells, the objective of this study was to evaluate the impact of DA on in vitro functional status of T cells from relapsing–remitting (RR)–MS patients. Peripheral T-cells from RR–MS patients were activated by mitogens and cell proliferation and cytokine production were assayed by [3 H]-thymidine uptake and ELISA, respectively. Our results demonstrated that DA enhanced in vitro T cell proliferation and Th17-related cytokines in MS-derived cell cultures. In addition, this catecholamine reduced Treg-related cytokines (IL-10 and TGF-β) release by activated CD4+ T cells. These DA-induced effects on T cells were mainly dependent on IL-6 production by both polyclonally-activated CD4+ T cells and LPS-stimulated monocytes. Furthermore, the production of IL-17 and IL-6 by MS-derived T cells was directly related with neurological disability (EDSS score), and the release of these cytokines was less sensitive to glucocorticoid inhibition in MS patients than in control group, mainly after DA addition. In conclusion, our data suggest that DA amplifies glucocorticoid-resistant Th17 phenotype in MS patients, and this phenomenon could be, at least in part, due to its ability to induce IL-6 production by monocytes and CD4+ T cells.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>24882215</pmid><doi>10.1016/j.bbi.2014.05.013</doi><tpages>9</tpages></addata></record> |
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| subjects | Adult Allergy and Immunology CD4-Positive T-Lymphocytes - drug effects CD4-Positive T-Lymphocytes - metabolism Cell Division Cells, Cultured Cytokines Dopamine Dopamine - pharmacology Drug Resistance Female Humans IL-10 Interleukin-10 - biosynthesis Interleukin-10 - genetics Interleukin-6 - biosynthesis Interleukin-6 - genetics Lipopolysaccharide Lymphocyte Activation Male Middle Aged Monocytes - drug effects Monocytes - metabolism Multiple sclerosis Multiple Sclerosis, Relapsing-Remitting - immunology Multiple Sclerosis, Relapsing-Remitting - metabolism Neuroimmunomodulation - physiology Phytohemagglutinins - pharmacology Psychiatry Severity of Illness Index T cells Th17 Th17 Cells - immunology Transforming Growth Factor beta - biosynthesis Transforming Growth Factor beta - genetics Young Adult |
| title | Dopamine favors expansion of glucocorticoid-resistant IL-17-producing T cells in multiple sclerosis |
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