Fingolimod increases CD39-expressing regulatory T cells in multiple sclerosis patients
Multiple sclerosis (MS) likely results from an imbalance between regulatory and inflammatory immune processes. CD39 is an ectoenzyme that cleaves ATP to AMP and has been suggested as a novel regulatory T cells (Treg) marker. As ATP has numerous proinflammatory effects, its degradation by CD39 has an...
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| creator | Muls, Nathalie Dang, Hong Anh Sindic, Christian J M van Pesch, Vincent |
| description | Multiple sclerosis (MS) likely results from an imbalance between regulatory and inflammatory immune processes. CD39 is an ectoenzyme that cleaves ATP to AMP and has been suggested as a novel regulatory T cells (Treg) marker. As ATP has numerous proinflammatory effects, its degradation by CD39 has anti-inflammatory influence. The purpose of this study was to explore regulatory and inflammatory mechanisms activated in fingolimod treated MS patients.
Peripheral blood mononuclear cells (PBMCs) were isolated from relapsing-remitting MS patients before starting fingolimod and three months after therapy start. mRNA expression was assessed in ex vivo PBMCs. The proportions of CD8, B cells, CD4 and CD39-expressing cells were analysed by flow cytometry. Treg proportion was quantified by flow cytometry and methylation-specific qPCR. Fingolimod treatment increased mRNA levels of CD39, AHR and CYP1B1 but decreased mRNA expression of IL-17, IL-22 and FOXP3 mRNA in PBMCs. B cells, CD4+ cells and Treg proportions were significantly reduced by this treatment, but remaining CD4+ T cells were enriched in FOXP3+ cells and in CD39-expressing Tregs.
In addition to the decrease in circulating CD4+ T cells and CD19+ B cells, our findings highlight additional immunoregulatory mechanisms induced by fingolimod. |
| doi_str_mv | 10.1371/journal.pone.0113025 |
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Peripheral blood mononuclear cells (PBMCs) were isolated from relapsing-remitting MS patients before starting fingolimod and three months after therapy start. mRNA expression was assessed in ex vivo PBMCs. The proportions of CD8, B cells, CD4 and CD39-expressing cells were analysed by flow cytometry. Treg proportion was quantified by flow cytometry and methylation-specific qPCR. Fingolimod treatment increased mRNA levels of CD39, AHR and CYP1B1 but decreased mRNA expression of IL-17, IL-22 and FOXP3 mRNA in PBMCs. B cells, CD4+ cells and Treg proportions were significantly reduced by this treatment, but remaining CD4+ T cells were enriched in FOXP3+ cells and in CD39-expressing Tregs.
In addition to the decrease in circulating CD4+ T cells and CD19+ B cells, our findings highlight additional immunoregulatory mechanisms induced by fingolimod.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0113025</identifier><identifier>PMID: 25411844</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>AMP ; Antigens, CD - genetics ; Antigens, CD - metabolism ; Antigens, CD19 - metabolism ; Apyrase - genetics ; Apyrase - metabolism ; ATP ; B cells ; B-Lymphocytes - metabolism ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Biology and life sciences ; Care and treatment ; CD19 antigen ; CD4 antigen ; CD4-Positive T-Lymphocytes - metabolism ; CD8 antigen ; Cytochrome P-450 CYP1B1 - genetics ; Cytokines ; Cytokines - metabolism ; Cytometry ; Deoxyribonucleic acid ; Dioxins ; DNA ; DNA methylation ; Fingolimod Hydrochloride - administration & dosage ; Fingolimod Hydrochloride - pharmacology ; Flow cytometry ; Foxp3 protein ; Gene expression ; Gene Expression Regulation - drug effects ; Humans ; Hydrocarbons ; Immunoregulation ; Immunosuppressive Agents - administration & dosage ; Immunosuppressive Agents - pharmacology ; Inflammation ; Interleukin 17 ; Interleukin 22 ; Kinases ; Leukocytes (mononuclear) ; Life sciences ; Lymphocytes ; Lymphocytes B ; Lymphocytes T ; Medicine and Health Sciences ; Memory ; Methylation ; Multiple sclerosis ; Multiple Sclerosis - drug therapy ; Multiple Sclerosis - genetics ; Multiple Sclerosis - immunology ; Neurochemistry ; Neurosciences ; Patients ; Peripheral blood mononuclear cells ; Receptors, Aryl Hydrocarbon - genetics ; RNA ; Statistical analysis ; T cells ; T-Lymphocytes, Regulatory - metabolism ; Thermal cycling ; Transcription factors</subject><ispartof>PloS one, 2014-11, Vol.9 (11), p.e113025-e113025</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Muls et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Muls et al 2014 Muls et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-6089abb00a80dbb74124686090bfb0f4d3bff46615e7473685cddcb4f71c55e53</citedby><cites>FETCH-LOGICAL-c692t-6089abb00a80dbb74124686090bfb0f4d3bff46615e7473685cddcb4f71c55e53</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/PMC4239031/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239031/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25411844$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Weber, Martin Sebastian</contributor><creatorcontrib>Muls, Nathalie</creatorcontrib><creatorcontrib>Dang, Hong Anh</creatorcontrib><creatorcontrib>Sindic, Christian J M</creatorcontrib><creatorcontrib>van Pesch, Vincent</creatorcontrib><title>Fingolimod increases CD39-expressing regulatory T cells in multiple sclerosis patients</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Multiple sclerosis (MS) likely results from an imbalance between regulatory and inflammatory immune processes. CD39 is an ectoenzyme that cleaves ATP to AMP and has been suggested as a novel regulatory T cells (Treg) marker. As ATP has numerous proinflammatory effects, its degradation by CD39 has anti-inflammatory influence. The purpose of this study was to explore regulatory and inflammatory mechanisms activated in fingolimod treated MS patients.
Peripheral blood mononuclear cells (PBMCs) were isolated from relapsing-remitting MS patients before starting fingolimod and three months after therapy start. mRNA expression was assessed in ex vivo PBMCs. The proportions of CD8, B cells, CD4 and CD39-expressing cells were analysed by flow cytometry. Treg proportion was quantified by flow cytometry and methylation-specific qPCR. Fingolimod treatment increased mRNA levels of CD39, AHR and CYP1B1 but decreased mRNA expression of IL-17, IL-22 and FOXP3 mRNA in PBMCs. B cells, CD4+ cells and Treg proportions were significantly reduced by this treatment, but remaining CD4+ T cells were enriched in FOXP3+ cells and in CD39-expressing Tregs.
In addition to the decrease in circulating CD4+ T cells and CD19+ B cells, our findings highlight additional immunoregulatory mechanisms induced by fingolimod.</description><subject>AMP</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, CD - metabolism</subject><subject>Antigens, CD19 - metabolism</subject><subject>Apyrase - genetics</subject><subject>Apyrase - metabolism</subject><subject>ATP</subject><subject>B cells</subject><subject>B-Lymphocytes - metabolism</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Biology and life sciences</subject><subject>Care and treatment</subject><subject>CD19 antigen</subject><subject>CD4 antigen</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>CD8 antigen</subject><subject>Cytochrome P-450 CYP1B1 - genetics</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Cytometry</subject><subject>Deoxyribonucleic acid</subject><subject>Dioxins</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>Fingolimod Hydrochloride - administration & dosage</subject><subject>Fingolimod Hydrochloride - pharmacology</subject><subject>Flow cytometry</subject><subject>Foxp3 protein</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Humans</subject><subject>Hydrocarbons</subject><subject>Immunoregulation</subject><subject>Immunosuppressive Agents - administration & dosage</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Inflammation</subject><subject>Interleukin 17</subject><subject>Interleukin 22</subject><subject>Kinases</subject><subject>Leukocytes (mononuclear)</subject><subject>Life sciences</subject><subject>Lymphocytes</subject><subject>Lymphocytes B</subject><subject>Lymphocytes T</subject><subject>Medicine and Health Sciences</subject><subject>Memory</subject><subject>Methylation</subject><subject>Multiple sclerosis</subject><subject>Multiple Sclerosis - drug therapy</subject><subject>Multiple Sclerosis - genetics</subject><subject>Multiple Sclerosis - immunology</subject><subject>Neurochemistry</subject><subject>Neurosciences</subject><subject>Patients</subject><subject>Peripheral blood mononuclear cells</subject><subject>Receptors, Aryl Hydrocarbon - genetics</subject><subject>RNA</subject><subject>Statistical analysis</subject><subject>T cells</subject><subject>T-Lymphocytes, Regulatory - metabolism</subject><subject>Thermal cycling</subject><subject>Transcription factors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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><sourceid>DOA</sourceid><recordid>eNqNksFu1DAQhiMEoqXwBggiISE47GLHjhNfkKothZUqVYLSq2U7k6xXThzsBLVvX283rTaoB-SDrfE3_3jGf5K8xWiJSYG_bN3oO2mXvetgiTAmKMufJceYk2zBMkSeH5yPklchbBHKScnYy-QoyynGJaXHyfW56RpnTeuq1HTagwwQ0tUZ4Qu46T2EEO9TD81o5eD8bXqVarA2RDhtRzuY3kIatAXvgglpLwcD3RBeJy9qaQO8mfaT5Pf5t6vVj8XF5ff16vRioRnPhgVDJZdKISRLVClVUJxRVjLEkaoVqmlFVF1TxnAOBS0IK3NdVVrRusA6zyEnJ8n7vW5vXRDTSILALGM5obzMIrHeE5WTW9F700p_K5w04j7gfCOkH0zsQKhCkopI0IQXNOclz0ASIBwrXiiKVdT6OlUbVQuVjp16aWei85vObETj_gqaEY4IjgKfJgHv_owQBtGasJun7MCN9-8uUFHwbId--Ad9uruJamRswHS1i3X1TlScUlxiwiktI7V8goqrgtbo6J_axPgs4fMsITID3AyNHEMQ618__5-9vJ6zHw_YDUg7bIKz42BcF-Yg3YM6-ip4qB-HjJHY2f9hGmJnfzHZP6a9O_ygx6QHv5M774f_ag</recordid><startdate>20141120</startdate><enddate>20141120</enddate><creator>Muls, Nathalie</creator><creator>Dang, Hong Anh</creator><creator>Sindic, Christian J M</creator><creator>van Pesch, Vincent</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20141120</creationdate><title>Fingolimod increases CD39-expressing regulatory T cells in multiple sclerosis patients</title><author>Muls, Nathalie ; Dang, Hong Anh ; Sindic, Christian J M ; van Pesch, Vincent</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-6089abb00a80dbb74124686090bfb0f4d3bff46615e7473685cddcb4f71c55e53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>AMP</topic><topic>Antigens, CD - genetics</topic><topic>Antigens, CD - metabolism</topic><topic>Antigens, CD19 - metabolism</topic><topic>Apyrase - genetics</topic><topic>Apyrase - metabolism</topic><topic>ATP</topic><topic>B cells</topic><topic>B-Lymphocytes - metabolism</topic><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Biology and life sciences</topic><topic>Care and treatment</topic><topic>CD19 antigen</topic><topic>CD4 antigen</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>CD8 antigen</topic><topic>Cytochrome P-450 CYP1B1 - genetics</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Cytometry</topic><topic>Deoxyribonucleic acid</topic><topic>Dioxins</topic><topic>DNA</topic><topic>DNA methylation</topic><topic>Fingolimod Hydrochloride - administration & dosage</topic><topic>Fingolimod Hydrochloride - pharmacology</topic><topic>Flow cytometry</topic><topic>Foxp3 protein</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Humans</topic><topic>Hydrocarbons</topic><topic>Immunoregulation</topic><topic>Immunosuppressive Agents - administration & dosage</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Inflammation</topic><topic>Interleukin 17</topic><topic>Interleukin 22</topic><topic>Kinases</topic><topic>Leukocytes (mononuclear)</topic><topic>Life sciences</topic><topic>Lymphocytes</topic><topic>Lymphocytes B</topic><topic>Lymphocytes T</topic><topic>Medicine and Health Sciences</topic><topic>Memory</topic><topic>Methylation</topic><topic>Multiple sclerosis</topic><topic>Multiple Sclerosis - drug therapy</topic><topic>Multiple Sclerosis - genetics</topic><topic>Multiple Sclerosis - immunology</topic><topic>Neurochemistry</topic><topic>Neurosciences</topic><topic>Patients</topic><topic>Peripheral blood mononuclear cells</topic><topic>Receptors, Aryl Hydrocarbon - genetics</topic><topic>RNA</topic><topic>Statistical analysis</topic><topic>T cells</topic><topic>T-Lymphocytes, Regulatory - metabolism</topic><topic>Thermal cycling</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Muls, Nathalie</creatorcontrib><creatorcontrib>Dang, Hong Anh</creatorcontrib><creatorcontrib>Sindic, Christian J M</creatorcontrib><creatorcontrib>van Pesch, Vincent</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Muls, Nathalie</au><au>Dang, Hong Anh</au><au>Sindic, Christian J M</au><au>van Pesch, Vincent</au><au>Weber, Martin Sebastian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fingolimod increases CD39-expressing regulatory T cells in multiple sclerosis patients</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-11-20</date><risdate>2014</risdate><volume>9</volume><issue>11</issue><spage>e113025</spage><epage>e113025</epage><pages>e113025-e113025</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Multiple sclerosis (MS) likely results from an imbalance between regulatory and inflammatory immune processes. CD39 is an ectoenzyme that cleaves ATP to AMP and has been suggested as a novel regulatory T cells (Treg) marker. As ATP has numerous proinflammatory effects, its degradation by CD39 has anti-inflammatory influence. The purpose of this study was to explore regulatory and inflammatory mechanisms activated in fingolimod treated MS patients.
Peripheral blood mononuclear cells (PBMCs) were isolated from relapsing-remitting MS patients before starting fingolimod and three months after therapy start. mRNA expression was assessed in ex vivo PBMCs. The proportions of CD8, B cells, CD4 and CD39-expressing cells were analysed by flow cytometry. Treg proportion was quantified by flow cytometry and methylation-specific qPCR. Fingolimod treatment increased mRNA levels of CD39, AHR and CYP1B1 but decreased mRNA expression of IL-17, IL-22 and FOXP3 mRNA in PBMCs. B cells, CD4+ cells and Treg proportions were significantly reduced by this treatment, but remaining CD4+ T cells were enriched in FOXP3+ cells and in CD39-expressing Tregs.
In addition to the decrease in circulating CD4+ T cells and CD19+ B cells, our findings highlight additional immunoregulatory mechanisms induced by fingolimod.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25411844</pmid><doi>10.1371/journal.pone.0113025</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | AMP Antigens, CD - genetics Antigens, CD - metabolism Antigens, CD19 - metabolism Apyrase - genetics Apyrase - metabolism ATP B cells B-Lymphocytes - metabolism Basic Helix-Loop-Helix Transcription Factors - genetics Biology and life sciences Care and treatment CD19 antigen CD4 antigen CD4-Positive T-Lymphocytes - metabolism CD8 antigen Cytochrome P-450 CYP1B1 - genetics Cytokines Cytokines - metabolism Cytometry Deoxyribonucleic acid Dioxins DNA DNA methylation Fingolimod Hydrochloride - administration & dosage Fingolimod Hydrochloride - pharmacology Flow cytometry Foxp3 protein Gene expression Gene Expression Regulation - drug effects Humans Hydrocarbons Immunoregulation Immunosuppressive Agents - administration & dosage Immunosuppressive Agents - pharmacology Inflammation Interleukin 17 Interleukin 22 Kinases Leukocytes (mononuclear) Life sciences Lymphocytes Lymphocytes B Lymphocytes T Medicine and Health Sciences Memory Methylation Multiple sclerosis Multiple Sclerosis - drug therapy Multiple Sclerosis - genetics Multiple Sclerosis - immunology Neurochemistry Neurosciences Patients Peripheral blood mononuclear cells Receptors, Aryl Hydrocarbon - genetics RNA Statistical analysis T cells T-Lymphocytes, Regulatory - metabolism Thermal cycling Transcription factors |
| title | Fingolimod increases CD39-expressing regulatory T cells in multiple sclerosis patients |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-29T00%3A39%3A17IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Fingolimod%20increases%20CD39-expressing%20regulatory%20T%20cells%20in%20multiple%20sclerosis%20patients&rft.jtitle=PloS%20one&rft.au=Muls,%20Nathalie&rft.date=2014-11-20&rft.volume=9&rft.issue=11&rft.spage=e113025&rft.epage=e113025&rft.pages=e113025-e113025&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0113025&rft_dat=%3Cgale_plos_%3EA418139448%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1626534982&rft_id=info:pmid/25411844&rft_galeid=A418139448&rft_doaj_id=oai_doaj_org_article_b7a3d3aec397459892ea3e391b97b41b&rfr_iscdi=true |