MBD2 regulates TH17 differentiation and experimental autoimmune encephalomyelitis by controlling the homeostasis of T-bet/Hlx axis
Abstract Unlike genetic alterations, epigenetic modifications are reversible and amenable to pharmacological interventions, which make them appealing targets for clinical therapy. However, little is known about epigenetic regulation in experimental autoimmune encephalomyelitis (EAE). Here we demonst...
Gespeichert in:
| Veröffentlicht in: | Journal of autoimmunity 2014-09, Vol.53, p.95-104 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 104 |
|---|---|
| container_issue | |
| container_start_page | 95 |
| container_title | Journal of autoimmunity |
| container_volume | 53 |
| creator | Zhong, Jixin Yu, Qilin Yang, Ping Rao, Xiaoquan He, Long Fang, Jing Tu, Yaqin Zhang, Zhijun Lai, Qiaohong Zhang, Shu Kuczma, Michal Kraj, Piatr Xu, Jun-Fa Gong, Feili Zhou, Jianfeng Wen, Li Eizirik, Decio L Du, Jie Wang, Wei Wang, Cong-Yi |
| description | Abstract Unlike genetic alterations, epigenetic modifications are reversible and amenable to pharmacological interventions, which make them appealing targets for clinical therapy. However, little is known about epigenetic regulation in experimental autoimmune encephalomyelitis (EAE). Here we demonstrated that methyl-CpG-binding domain protein 2 (MBD2), an epigenetic regulator, controls autoimmunity and EAE through T-bet/Hlx. Tbx21 and Hlx underwent a DNA methylation turnover upon polarizations and a unique methylation pattern was essential for TH 17 development. Loss of Mbd2 resulted in a defect for reading the information encoded by this methylation turnover, which disrupted the homeostasis of T-bet/Hlx axis and suppressed TH 17 differentiation. DNA demethylation induced similar effect on helper T cell differentiation. Therefore, Mbd2 −/− mice were completely protected from EAE. Pathogenic splenocytes isolated from wild-type mice challenged with MOG35-55 could adoptively transfer disease to Mbd2 −/− mice. In addition, Mbd2 −/− mice reconstituted with unstimulated wild-type splenocytes developed EAE as wild-type mice did. These data would provide novel insights into epigenetic regulation of EAE. |
| doi_str_mv | 10.1016/j.jaut.2014.05.006 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1635030157</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S089684111400095X</els_id><sourcerecordid>1561969240</sourcerecordid><originalsourceid>FETCH-LOGICAL-c459t-3ec8a291ec34429602b2446216a7fb81ed483e47be3486bdba3ceacbbf0171a13</originalsourceid><addsrcrecordid>eNqFkkuLFDEQgIMo7rj6BzxILoKX7k2l0y8QQdfHCCseHMFbSKerdzKmO2OSlpmrv9w0Myp40FOg8tWD-oqQx8ByYFBd7fKdmmPOGYiclTlj1R2yAtaWWQtlfZesWNNWWSMALsiDEHaMAZRleZ9ccNEWomybFfnx4dVrTj3ezlZFDHSzhpr2ZhjQ4xSNisZNVE09xcMevRlTUFma2jozjvOEFCeN-62ybjyiNdEE2h2pdlP0zloz3dK4Rbp1I7oQVUjfbqCbrMN4tbYHqg4mPCT3BmUDPjq_l-Tz2zeb63V28_Hd--uXN5lOo8asQN0o3gLqQgjeVox3XIiKQ6XqoWsAe9EUKOoOC9FUXd-pQqPSXTcwqEFBcUmeneruvfs2Y4hyNEGjtWpCNwcJVVGygqXV_R8tK2irlguWUH5CtXcheBzkPq1J-aMEJhdNcicXTXLRJFkpk6aU9ORcf-5G7H-n_PKSgKdnQAWt7ODVpE34wzV1zet26f78xGFa3HeDXgZtFiW98aij7J359xwv_krXyZlJHb_iEcPOzX5KSiTIwCWTn5aDWu4JBGPpzr4UPwH8X8c5</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1561969240</pqid></control><display><type>article</type><title>MBD2 regulates TH17 differentiation and experimental autoimmune encephalomyelitis by controlling the homeostasis of T-bet/Hlx axis</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Zhong, Jixin ; Yu, Qilin ; Yang, Ping ; Rao, Xiaoquan ; He, Long ; Fang, Jing ; Tu, Yaqin ; Zhang, Zhijun ; Lai, Qiaohong ; Zhang, Shu ; Kuczma, Michal ; Kraj, Piatr ; Xu, Jun-Fa ; Gong, Feili ; Zhou, Jianfeng ; Wen, Li ; Eizirik, Decio L ; Du, Jie ; Wang, Wei ; Wang, Cong-Yi</creator><creatorcontrib>Zhong, Jixin ; Yu, Qilin ; Yang, Ping ; Rao, Xiaoquan ; He, Long ; Fang, Jing ; Tu, Yaqin ; Zhang, Zhijun ; Lai, Qiaohong ; Zhang, Shu ; Kuczma, Michal ; Kraj, Piatr ; Xu, Jun-Fa ; Gong, Feili ; Zhou, Jianfeng ; Wen, Li ; Eizirik, Decio L ; Du, Jie ; Wang, Wei ; Wang, Cong-Yi</creatorcontrib><description>Abstract Unlike genetic alterations, epigenetic modifications are reversible and amenable to pharmacological interventions, which make them appealing targets for clinical therapy. However, little is known about epigenetic regulation in experimental autoimmune encephalomyelitis (EAE). Here we demonstrated that methyl-CpG-binding domain protein 2 (MBD2), an epigenetic regulator, controls autoimmunity and EAE through T-bet/Hlx. Tbx21 and Hlx underwent a DNA methylation turnover upon polarizations and a unique methylation pattern was essential for TH 17 development. Loss of Mbd2 resulted in a defect for reading the information encoded by this methylation turnover, which disrupted the homeostasis of T-bet/Hlx axis and suppressed TH 17 differentiation. DNA demethylation induced similar effect on helper T cell differentiation. Therefore, Mbd2 −/− mice were completely protected from EAE. Pathogenic splenocytes isolated from wild-type mice challenged with MOG35-55 could adoptively transfer disease to Mbd2 −/− mice. In addition, Mbd2 −/− mice reconstituted with unstimulated wild-type splenocytes developed EAE as wild-type mice did. These data would provide novel insights into epigenetic regulation of EAE.</description><identifier>ISSN: 0896-8411</identifier><identifier>EISSN: 1095-9157</identifier><identifier>DOI: 10.1016/j.jaut.2014.05.006</identifier><identifier>PMID: 24934598</identifier><language>eng</language><publisher>Kidlington: Elsevier Ltd</publisher><subject>Allergy and Immunology ; Animals ; Biological and medical sciences ; Cell Differentiation - genetics ; Cell Differentiation - immunology ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - immunology ; EAE ; Encephalomyelitis, Autoimmune, Experimental - chemically induced ; Encephalomyelitis, Autoimmune, Experimental - genetics ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Epigenesis, Genetic - genetics ; Epigenesis, Genetic - immunology ; Epigenetic ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Homeodomain Proteins - genetics ; Homeodomain Proteins - immunology ; MBD2 ; Medical sciences ; Methylation ; Mice ; Mice, Knockout ; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis ; Myelin-Oligodendrocyte Glycoprotein - toxicity ; Neurology ; Peptide Fragments - toxicity ; T-bet ; T-Box Domain Proteins - genetics ; T-Box Domain Proteins - immunology ; TH17 ; Th17 Cells - immunology ; Th17 Cells - pathology ; Transcription Factors - genetics ; Transcription Factors - immunology</subject><ispartof>Journal of autoimmunity, 2014-09, Vol.53, p.95-104</ispartof><rights>Elsevier Ltd</rights><rights>2014 Elsevier Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2014 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-3ec8a291ec34429602b2446216a7fb81ed483e47be3486bdba3ceacbbf0171a13</citedby><cites>FETCH-LOGICAL-c459t-3ec8a291ec34429602b2446216a7fb81ed483e47be3486bdba3ceacbbf0171a13</cites><orcidid>0000-0002-3534-7480</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jaut.2014.05.006$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28772790$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24934598$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhong, Jixin</creatorcontrib><creatorcontrib>Yu, Qilin</creatorcontrib><creatorcontrib>Yang, Ping</creatorcontrib><creatorcontrib>Rao, Xiaoquan</creatorcontrib><creatorcontrib>He, Long</creatorcontrib><creatorcontrib>Fang, Jing</creatorcontrib><creatorcontrib>Tu, Yaqin</creatorcontrib><creatorcontrib>Zhang, Zhijun</creatorcontrib><creatorcontrib>Lai, Qiaohong</creatorcontrib><creatorcontrib>Zhang, Shu</creatorcontrib><creatorcontrib>Kuczma, Michal</creatorcontrib><creatorcontrib>Kraj, Piatr</creatorcontrib><creatorcontrib>Xu, Jun-Fa</creatorcontrib><creatorcontrib>Gong, Feili</creatorcontrib><creatorcontrib>Zhou, Jianfeng</creatorcontrib><creatorcontrib>Wen, Li</creatorcontrib><creatorcontrib>Eizirik, Decio L</creatorcontrib><creatorcontrib>Du, Jie</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Wang, Cong-Yi</creatorcontrib><title>MBD2 regulates TH17 differentiation and experimental autoimmune encephalomyelitis by controlling the homeostasis of T-bet/Hlx axis</title><title>Journal of autoimmunity</title><addtitle>J Autoimmun</addtitle><description>Abstract Unlike genetic alterations, epigenetic modifications are reversible and amenable to pharmacological interventions, which make them appealing targets for clinical therapy. However, little is known about epigenetic regulation in experimental autoimmune encephalomyelitis (EAE). Here we demonstrated that methyl-CpG-binding domain protein 2 (MBD2), an epigenetic regulator, controls autoimmunity and EAE through T-bet/Hlx. Tbx21 and Hlx underwent a DNA methylation turnover upon polarizations and a unique methylation pattern was essential for TH 17 development. Loss of Mbd2 resulted in a defect for reading the information encoded by this methylation turnover, which disrupted the homeostasis of T-bet/Hlx axis and suppressed TH 17 differentiation. DNA demethylation induced similar effect on helper T cell differentiation. Therefore, Mbd2 −/− mice were completely protected from EAE. Pathogenic splenocytes isolated from wild-type mice challenged with MOG35-55 could adoptively transfer disease to Mbd2 −/− mice. In addition, Mbd2 −/− mice reconstituted with unstimulated wild-type splenocytes developed EAE as wild-type mice did. These data would provide novel insights into epigenetic regulation of EAE.</description><subject>Allergy and Immunology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation - genetics</subject><subject>Cell Differentiation - immunology</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - immunology</subject><subject>EAE</subject><subject>Encephalomyelitis, Autoimmune, Experimental - chemically induced</subject><subject>Encephalomyelitis, Autoimmune, Experimental - genetics</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Epigenesis, Genetic - genetics</subject><subject>Epigenesis, Genetic - immunology</subject><subject>Epigenetic</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - immunology</subject><subject>MBD2</subject><subject>Medical sciences</subject><subject>Methylation</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</subject><subject>Myelin-Oligodendrocyte Glycoprotein - toxicity</subject><subject>Neurology</subject><subject>Peptide Fragments - toxicity</subject><subject>T-bet</subject><subject>T-Box Domain Proteins - genetics</subject><subject>T-Box Domain Proteins - immunology</subject><subject>TH17</subject><subject>Th17 Cells - immunology</subject><subject>Th17 Cells - pathology</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - immunology</subject><issn>0896-8411</issn><issn>1095-9157</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkkuLFDEQgIMo7rj6BzxILoKX7k2l0y8QQdfHCCseHMFbSKerdzKmO2OSlpmrv9w0Myp40FOg8tWD-oqQx8ByYFBd7fKdmmPOGYiclTlj1R2yAtaWWQtlfZesWNNWWSMALsiDEHaMAZRleZ9ccNEWomybFfnx4dVrTj3ezlZFDHSzhpr2ZhjQ4xSNisZNVE09xcMevRlTUFma2jozjvOEFCeN-62ybjyiNdEE2h2pdlP0zloz3dK4Rbp1I7oQVUjfbqCbrMN4tbYHqg4mPCT3BmUDPjq_l-Tz2zeb63V28_Hd--uXN5lOo8asQN0o3gLqQgjeVox3XIiKQ6XqoWsAe9EUKOoOC9FUXd-pQqPSXTcwqEFBcUmeneruvfs2Y4hyNEGjtWpCNwcJVVGygqXV_R8tK2irlguWUH5CtXcheBzkPq1J-aMEJhdNcicXTXLRJFkpk6aU9ORcf-5G7H-n_PKSgKdnQAWt7ODVpE34wzV1zet26f78xGFa3HeDXgZtFiW98aij7J359xwv_krXyZlJHb_iEcPOzX5KSiTIwCWTn5aDWu4JBGPpzr4UPwH8X8c5</recordid><startdate>201409</startdate><enddate>201409</enddate><creator>Zhong, Jixin</creator><creator>Yu, Qilin</creator><creator>Yang, Ping</creator><creator>Rao, Xiaoquan</creator><creator>He, Long</creator><creator>Fang, Jing</creator><creator>Tu, Yaqin</creator><creator>Zhang, Zhijun</creator><creator>Lai, Qiaohong</creator><creator>Zhang, Shu</creator><creator>Kuczma, Michal</creator><creator>Kraj, Piatr</creator><creator>Xu, Jun-Fa</creator><creator>Gong, Feili</creator><creator>Zhou, Jianfeng</creator><creator>Wen, Li</creator><creator>Eizirik, Decio L</creator><creator>Du, Jie</creator><creator>Wang, Wei</creator><creator>Wang, Cong-Yi</creator><general>Elsevier Ltd</general><general>Elsevier</general><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>7X8</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><orcidid>https://orcid.org/0000-0002-3534-7480</orcidid></search><sort><creationdate>201409</creationdate><title>MBD2 regulates TH17 differentiation and experimental autoimmune encephalomyelitis by controlling the homeostasis of T-bet/Hlx axis</title><author>Zhong, Jixin ; Yu, Qilin ; Yang, Ping ; Rao, Xiaoquan ; He, Long ; Fang, Jing ; Tu, Yaqin ; Zhang, Zhijun ; Lai, Qiaohong ; Zhang, Shu ; Kuczma, Michal ; Kraj, Piatr ; Xu, Jun-Fa ; Gong, Feili ; Zhou, Jianfeng ; Wen, Li ; Eizirik, Decio L ; Du, Jie ; Wang, Wei ; Wang, Cong-Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-3ec8a291ec34429602b2446216a7fb81ed483e47be3486bdba3ceacbbf0171a13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Allergy and Immunology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation - genetics</topic><topic>Cell Differentiation - immunology</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - immunology</topic><topic>EAE</topic><topic>Encephalomyelitis, Autoimmune, Experimental - chemically induced</topic><topic>Encephalomyelitis, Autoimmune, Experimental - genetics</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Epigenesis, Genetic - genetics</topic><topic>Epigenesis, Genetic - immunology</topic><topic>Epigenetic</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - immunology</topic><topic>MBD2</topic><topic>Medical sciences</topic><topic>Methylation</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</topic><topic>Myelin-Oligodendrocyte Glycoprotein - toxicity</topic><topic>Neurology</topic><topic>Peptide Fragments - toxicity</topic><topic>T-bet</topic><topic>T-Box Domain Proteins - genetics</topic><topic>T-Box Domain Proteins - immunology</topic><topic>TH17</topic><topic>Th17 Cells - immunology</topic><topic>Th17 Cells - pathology</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhong, Jixin</creatorcontrib><creatorcontrib>Yu, Qilin</creatorcontrib><creatorcontrib>Yang, Ping</creatorcontrib><creatorcontrib>Rao, Xiaoquan</creatorcontrib><creatorcontrib>He, Long</creatorcontrib><creatorcontrib>Fang, Jing</creatorcontrib><creatorcontrib>Tu, Yaqin</creatorcontrib><creatorcontrib>Zhang, Zhijun</creatorcontrib><creatorcontrib>Lai, Qiaohong</creatorcontrib><creatorcontrib>Zhang, Shu</creatorcontrib><creatorcontrib>Kuczma, Michal</creatorcontrib><creatorcontrib>Kraj, Piatr</creatorcontrib><creatorcontrib>Xu, Jun-Fa</creatorcontrib><creatorcontrib>Gong, Feili</creatorcontrib><creatorcontrib>Zhou, Jianfeng</creatorcontrib><creatorcontrib>Wen, Li</creatorcontrib><creatorcontrib>Eizirik, Decio L</creatorcontrib><creatorcontrib>Du, Jie</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Wang, Cong-Yi</creatorcontrib><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>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of autoimmunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhong, Jixin</au><au>Yu, Qilin</au><au>Yang, Ping</au><au>Rao, Xiaoquan</au><au>He, Long</au><au>Fang, Jing</au><au>Tu, Yaqin</au><au>Zhang, Zhijun</au><au>Lai, Qiaohong</au><au>Zhang, Shu</au><au>Kuczma, Michal</au><au>Kraj, Piatr</au><au>Xu, Jun-Fa</au><au>Gong, Feili</au><au>Zhou, Jianfeng</au><au>Wen, Li</au><au>Eizirik, Decio L</au><au>Du, Jie</au><au>Wang, Wei</au><au>Wang, Cong-Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MBD2 regulates TH17 differentiation and experimental autoimmune encephalomyelitis by controlling the homeostasis of T-bet/Hlx axis</atitle><jtitle>Journal of autoimmunity</jtitle><addtitle>J Autoimmun</addtitle><date>2014-09</date><risdate>2014</risdate><volume>53</volume><spage>95</spage><epage>104</epage><pages>95-104</pages><issn>0896-8411</issn><eissn>1095-9157</eissn><abstract>Abstract Unlike genetic alterations, epigenetic modifications are reversible and amenable to pharmacological interventions, which make them appealing targets for clinical therapy. However, little is known about epigenetic regulation in experimental autoimmune encephalomyelitis (EAE). Here we demonstrated that methyl-CpG-binding domain protein 2 (MBD2), an epigenetic regulator, controls autoimmunity and EAE through T-bet/Hlx. Tbx21 and Hlx underwent a DNA methylation turnover upon polarizations and a unique methylation pattern was essential for TH 17 development. Loss of Mbd2 resulted in a defect for reading the information encoded by this methylation turnover, which disrupted the homeostasis of T-bet/Hlx axis and suppressed TH 17 differentiation. DNA demethylation induced similar effect on helper T cell differentiation. Therefore, Mbd2 −/− mice were completely protected from EAE. Pathogenic splenocytes isolated from wild-type mice challenged with MOG35-55 could adoptively transfer disease to Mbd2 −/− mice. In addition, Mbd2 −/− mice reconstituted with unstimulated wild-type splenocytes developed EAE as wild-type mice did. These data would provide novel insights into epigenetic regulation of EAE.</abstract><cop>Kidlington</cop><pub>Elsevier Ltd</pub><pmid>24934598</pmid><doi>10.1016/j.jaut.2014.05.006</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-3534-7480</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0896-8411 |
| ispartof | Journal of autoimmunity, 2014-09, Vol.53, p.95-104 |
| issn | 0896-8411 1095-9157 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1635030157 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Allergy and Immunology Animals Biological and medical sciences Cell Differentiation - genetics Cell Differentiation - immunology DNA-Binding Proteins - genetics DNA-Binding Proteins - immunology EAE Encephalomyelitis, Autoimmune, Experimental - chemically induced Encephalomyelitis, Autoimmune, Experimental - genetics Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - pathology Epigenesis, Genetic - genetics Epigenesis, Genetic - immunology Epigenetic Fundamental and applied biological sciences. Psychology Fundamental immunology Homeodomain Proteins - genetics Homeodomain Proteins - immunology MBD2 Medical sciences Methylation Mice Mice, Knockout Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Myelin-Oligodendrocyte Glycoprotein - toxicity Neurology Peptide Fragments - toxicity T-bet T-Box Domain Proteins - genetics T-Box Domain Proteins - immunology TH17 Th17 Cells - immunology Th17 Cells - pathology Transcription Factors - genetics Transcription Factors - immunology |
| title | MBD2 regulates TH17 differentiation and experimental autoimmune encephalomyelitis by controlling the homeostasis of T-bet/Hlx axis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T02%3A18%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=MBD2%20regulates%20TH17%20differentiation%20and%20experimental%20autoimmune%20encephalomyelitis%20by%20controlling%20the%20homeostasis%20of%20T-bet/Hlx%20axis&rft.jtitle=Journal%20of%20autoimmunity&rft.au=Zhong,%20Jixin&rft.date=2014-09&rft.volume=53&rft.spage=95&rft.epage=104&rft.pages=95-104&rft.issn=0896-8411&rft.eissn=1095-9157&rft_id=info:doi/10.1016/j.jaut.2014.05.006&rft_dat=%3Cproquest_cross%3E1561969240%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1561969240&rft_id=info:pmid/24934598&rft_els_id=S089684111400095X&rfr_iscdi=true |