RORγt, but not T-bet, overexpression exacerbates an autoimmune model for multiple sclerosis
Abstract Th17 cells play an important role in multiple sclerosis (MS) and its autoimmune model, experimental autoimmune encephalomyelitis (EAE). However, studies have not addressed how enhanced Th17 immune responses can affect demyelinating diseases. We induced EAE with MOG in RORγt transgenic C57BL...
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| Veröffentlicht in: | Journal of neuroimmunology 2014-11, Vol.276 (1), p.142-149 |
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| container_title | Journal of neuroimmunology |
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| creator | Martinez, Nicholas E Sato, Fumitaka Omura, Seiichi Kawai, Eiichiro Takahashi, Satoru Yoh, Keigyou Tsunoda, Ikuo |
| description | Abstract Th17 cells play an important role in multiple sclerosis (MS) and its autoimmune model, experimental autoimmune encephalomyelitis (EAE). However, studies have not addressed how enhanced Th17 immune responses can affect demyelinating diseases. We induced EAE with MOG in RORγt transgenic C57BL/6 mice that overexpress a Th17 inducing transcription factor. RORγt transgenic mice developed more severe EAE than wild-type mice with more robust anti-MOG Th17 immune responses. In contrast, mice overexpressing T-bet, a Th1-inducing transcription factor, were resistant to EAE. Therefore, a genetic bias toward Th17 immune responses could contribute to CNS immunopathology. |
| doi_str_mv | 10.1016/j.jneuroim.2014.09.006 |
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However, studies have not addressed how enhanced Th17 immune responses can affect demyelinating diseases. We induced EAE with MOG in RORγt transgenic C57BL/6 mice that overexpress a Th17 inducing transcription factor. RORγt transgenic mice developed more severe EAE than wild-type mice with more robust anti-MOG Th17 immune responses. In contrast, mice overexpressing T-bet, a Th1-inducing transcription factor, were resistant to EAE. Therefore, a genetic bias toward Th17 immune responses could contribute to CNS immunopathology.</description><identifier>ISSN: 0165-5728</identifier><identifier>EISSN: 1872-8421</identifier><identifier>DOI: 10.1016/j.jneuroim.2014.09.006</identifier><identifier>PMID: 25288300</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Allergy and Immunology ; Animals ; Autoimmune disease ; Cell Proliferation - drug effects ; Cell Proliferation - genetics ; Central Nervous System - metabolism ; Central Nervous System - pathology ; Demyelinating disease ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental - chemically induced ; Encephalomyelitis, Autoimmune, Experimental - genetics ; Flow Cytometry ; Gain-of-function ; Genetic association ; Leukocytes, Mononuclear - drug effects ; Leukocytes, Mononuclear - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Multiple Sclerosis - chemically induced ; Multiple Sclerosis - genetics ; Multiple Sclerosis - pathology ; Neurology ; Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics ; T cell differentiation ; T-Box Domain Proteins - genetics ; Th1 Cells - pathology</subject><ispartof>Journal of neuroimmunology, 2014-11, Vol.276 (1), p.142-149</ispartof><rights>Elsevier B.V.</rights><rights>2014 Elsevier B.V.</rights><rights>Copyright © 2014 Elsevier B.V. All rights reserved.</rights><rights>2014 Elsevier B.V. All rights reserved. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-97e7a5868f93df2f06ebb8c48d1f0635f53d642f564e4e8977dd362860bf56493</citedby><cites>FETCH-LOGICAL-c526t-97e7a5868f93df2f06ebb8c48d1f0635f53d642f564e4e8977dd362860bf56493</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jneuroim.2014.09.006$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,315,781,785,886,3551,27926,27927,45997</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25288300$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martinez, Nicholas E</creatorcontrib><creatorcontrib>Sato, Fumitaka</creatorcontrib><creatorcontrib>Omura, Seiichi</creatorcontrib><creatorcontrib>Kawai, Eiichiro</creatorcontrib><creatorcontrib>Takahashi, Satoru</creatorcontrib><creatorcontrib>Yoh, Keigyou</creatorcontrib><creatorcontrib>Tsunoda, Ikuo</creatorcontrib><title>RORγt, but not T-bet, overexpression exacerbates an autoimmune model for multiple sclerosis</title><title>Journal of neuroimmunology</title><addtitle>J Neuroimmunol</addtitle><description>Abstract Th17 cells play an important role in multiple sclerosis (MS) and its autoimmune model, experimental autoimmune encephalomyelitis (EAE). However, studies have not addressed how enhanced Th17 immune responses can affect demyelinating diseases. We induced EAE with MOG in RORγt transgenic C57BL/6 mice that overexpress a Th17 inducing transcription factor. RORγt transgenic mice developed more severe EAE than wild-type mice with more robust anti-MOG Th17 immune responses. In contrast, mice overexpressing T-bet, a Th1-inducing transcription factor, were resistant to EAE. Therefore, a genetic bias toward Th17 immune responses could contribute to CNS immunopathology.</description><subject>Allergy and Immunology</subject><subject>Animals</subject><subject>Autoimmune disease</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Proliferation - genetics</subject><subject>Central Nervous System - metabolism</subject><subject>Central Nervous System - pathology</subject><subject>Demyelinating disease</subject><subject>Disease Models, Animal</subject><subject>Encephalomyelitis, Autoimmune, Experimental - chemically induced</subject><subject>Encephalomyelitis, Autoimmune, Experimental - genetics</subject><subject>Flow Cytometry</subject><subject>Gain-of-function</subject><subject>Genetic association</subject><subject>Leukocytes, Mononuclear - drug effects</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Multiple Sclerosis - chemically induced</subject><subject>Multiple Sclerosis - genetics</subject><subject>Multiple Sclerosis - pathology</subject><subject>Neurology</subject><subject>Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics</subject><subject>T cell differentiation</subject><subject>T-Box Domain Proteins - genetics</subject><subject>Th1 Cells - pathology</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkVtu1TAURS0EopfCFCoPgAS_4jg_FajiJVWqVMofkuU4J-CQ2Fe2c9WOi3kwJhxdWgE_fPm1z97H6yB0RklNCZWvpnrysMbglpoRKmrS1YTIR2hHVcsqJRh9jHZF2FRNy9QJepbSRAhtuOieohPWMKU4ITv05frq-ueP_BL3a8Y-ZHxT9VCO4QARbvcRUnLBY7g1FmJvMiRsPDZrLsnL6gEvYYAZjyHiZZ2z28-Ak50hhuTSc_RkNHOCF7_XU_T53dubiw_V5dX7jxdvLivbMJmrroXWNEqqsePDyEYioe-VFWqgZc-bseGDFGxspAABqmvbYeCSKUn67a7jp-j86Ltf-wUGCz5HM-t9dIuJdzoYp_9-8e6b_hoOWhQQvKXFQB4NbOk7RRgfainRG2896XveeuOtSacL71J49mfyQ9k94CJ4fRRA-f_BQdTJOvAWBhfBZj0E9_-M838s7Oy8s2b-DneQprBGX-hqqhPTRH_apr4NnQpCShOM_wKcPa0p</recordid><startdate>20141115</startdate><enddate>20141115</enddate><creator>Martinez, Nicholas E</creator><creator>Sato, Fumitaka</creator><creator>Omura, Seiichi</creator><creator>Kawai, Eiichiro</creator><creator>Takahashi, Satoru</creator><creator>Yoh, Keigyou</creator><creator>Tsunoda, Ikuo</creator><general>Elsevier B.V</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>5PM</scope></search><sort><creationdate>20141115</creationdate><title>RORγt, but not T-bet, overexpression exacerbates an autoimmune model for multiple sclerosis</title><author>Martinez, Nicholas E ; Sato, Fumitaka ; Omura, Seiichi ; Kawai, Eiichiro ; Takahashi, Satoru ; Yoh, Keigyou ; Tsunoda, Ikuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-97e7a5868f93df2f06ebb8c48d1f0635f53d642f564e4e8977dd362860bf56493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Allergy and Immunology</topic><topic>Animals</topic><topic>Autoimmune disease</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Proliferation - genetics</topic><topic>Central Nervous System - metabolism</topic><topic>Central Nervous System - pathology</topic><topic>Demyelinating disease</topic><topic>Disease Models, Animal</topic><topic>Encephalomyelitis, Autoimmune, Experimental - chemically induced</topic><topic>Encephalomyelitis, Autoimmune, Experimental - genetics</topic><topic>Flow Cytometry</topic><topic>Gain-of-function</topic><topic>Genetic association</topic><topic>Leukocytes, Mononuclear - drug effects</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Multiple Sclerosis - chemically induced</topic><topic>Multiple Sclerosis - genetics</topic><topic>Multiple Sclerosis - pathology</topic><topic>Neurology</topic><topic>Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics</topic><topic>T cell differentiation</topic><topic>T-Box Domain Proteins - genetics</topic><topic>Th1 Cells - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martinez, Nicholas E</creatorcontrib><creatorcontrib>Sato, Fumitaka</creatorcontrib><creatorcontrib>Omura, Seiichi</creatorcontrib><creatorcontrib>Kawai, Eiichiro</creatorcontrib><creatorcontrib>Takahashi, Satoru</creatorcontrib><creatorcontrib>Yoh, Keigyou</creatorcontrib><creatorcontrib>Tsunoda, Ikuo</creatorcontrib><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>Journal of neuroimmunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martinez, Nicholas E</au><au>Sato, Fumitaka</au><au>Omura, Seiichi</au><au>Kawai, Eiichiro</au><au>Takahashi, Satoru</au><au>Yoh, Keigyou</au><au>Tsunoda, Ikuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RORγt, but not T-bet, overexpression exacerbates an autoimmune model for multiple sclerosis</atitle><jtitle>Journal of neuroimmunology</jtitle><addtitle>J Neuroimmunol</addtitle><date>2014-11-15</date><risdate>2014</risdate><volume>276</volume><issue>1</issue><spage>142</spage><epage>149</epage><pages>142-149</pages><issn>0165-5728</issn><eissn>1872-8421</eissn><abstract>Abstract Th17 cells play an important role in multiple sclerosis (MS) and its autoimmune model, experimental autoimmune encephalomyelitis (EAE). However, studies have not addressed how enhanced Th17 immune responses can affect demyelinating diseases. We induced EAE with MOG in RORγt transgenic C57BL/6 mice that overexpress a Th17 inducing transcription factor. RORγt transgenic mice developed more severe EAE than wild-type mice with more robust anti-MOG Th17 immune responses. In contrast, mice overexpressing T-bet, a Th1-inducing transcription factor, were resistant to EAE. Therefore, a genetic bias toward Th17 immune responses could contribute to CNS immunopathology.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>25288300</pmid><doi>10.1016/j.jneuroim.2014.09.006</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Allergy and Immunology Animals Autoimmune disease Cell Proliferation - drug effects Cell Proliferation - genetics Central Nervous System - metabolism Central Nervous System - pathology Demyelinating disease Disease Models, Animal Encephalomyelitis, Autoimmune, Experimental - chemically induced Encephalomyelitis, Autoimmune, Experimental - genetics Flow Cytometry Gain-of-function Genetic association Leukocytes, Mononuclear - drug effects Leukocytes, Mononuclear - metabolism Mice Mice, Inbred C57BL Mice, Transgenic Multiple Sclerosis - chemically induced Multiple Sclerosis - genetics Multiple Sclerosis - pathology Neurology Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics T cell differentiation T-Box Domain Proteins - genetics Th1 Cells - pathology |
| title | RORγt, but not T-bet, overexpression exacerbates an autoimmune model for multiple sclerosis |
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