T Helper 17 Lineage Differentiation Is Programmed by Orphan Nuclear Receptors ROR[alpha] and ROR[gamma]
T cell functional differentiation is mediated by lineage-specific transcription factors. T helper 17 (Th17) has been recently identified as a distinct Th lineage mediating tissue inflammation. Retinoic acid receptor-related orphan receptor γ (RORγ) was shown to regulate Th17 differentiation; RORγ de...
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| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2008-01, Vol.28 (1), p.29 |
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| creator | Yang, Xuexian O Pappu, Bhanu P Nurieva, Roza Akimzhanov, Askar Kang, Hong Soon Chung, Yeonseok Ma, Li Shah, Bhavin Panopoulos, Athanasia D Schluns, Kimberly S Watowich, Stephanie S Tian, Qiang Jetten, Anton M Dong, Chen |
| description | T cell functional differentiation is mediated by lineage-specific transcription factors. T helper 17 (Th17) has been recently identified as a distinct Th lineage mediating tissue inflammation. Retinoic acid receptor-related orphan receptor γ (RORγ) was shown to regulate Th17 differentiation; RORγ deficiency, however, did not completely abolish Th17 cytokine expression. Here, we report Th17 cells highly expressed another related nuclear receptor, RORα, induced by transforming growth factor-β and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3. Overexpression of RORα promoted Th17 differentiation, possibly through the conserved noncoding sequence 2 inIl17-Il17flocus. RORα deficiency resulted in reduced IL-17 expressionin vitroandin vivo. Furthermore, RORα and RORγ coexpression synergistically led to greater Th17 differentiation. Double deficiencies in RORα and RORγ globally impaired Th17 generation and completely protected mice against experimental autoimmune encephalomyelitis. Therefore, Th17 differentiation is directed by two lineage-specific nuclear receptors, RORα and RORγ. |
| doi_str_mv | 10.1016/j.immuni.2007.11.016 |
| format | Article |
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T helper 17 (Th17) has been recently identified as a distinct Th lineage mediating tissue inflammation. Retinoic acid receptor-related orphan receptor γ (RORγ) was shown to regulate Th17 differentiation; RORγ deficiency, however, did not completely abolish Th17 cytokine expression. Here, we report Th17 cells highly expressed another related nuclear receptor, RORα, induced by transforming growth factor-β and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3. Overexpression of RORα promoted Th17 differentiation, possibly through the conserved noncoding sequence 2 inIl17-Il17flocus. RORα deficiency resulted in reduced IL-17 expressionin vitroandin vivo. Furthermore, RORα and RORγ coexpression synergistically led to greater Th17 differentiation. Double deficiencies in RORα and RORγ globally impaired Th17 generation and completely protected mice against experimental autoimmune encephalomyelitis. Therefore, Th17 differentiation is directed by two lineage-specific nuclear receptors, RORα and RORγ.</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2007.11.016</identifier><language>eng</language><publisher>Cambridge: Elsevier Limited</publisher><subject>Cancer ; Deoxyribonucleic acid ; DNA ; Gene expression ; Lymphocytes ; Medical research ; Rodents ; Transcription factors</subject><ispartof>Immunity (Cambridge, Mass.), 2008-01, Vol.28 (1), p.29</ispartof><rights>Copyright Elsevier Limited Jan 18, 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Yang, Xuexian O</creatorcontrib><creatorcontrib>Pappu, Bhanu P</creatorcontrib><creatorcontrib>Nurieva, Roza</creatorcontrib><creatorcontrib>Akimzhanov, Askar</creatorcontrib><creatorcontrib>Kang, Hong Soon</creatorcontrib><creatorcontrib>Chung, Yeonseok</creatorcontrib><creatorcontrib>Ma, Li</creatorcontrib><creatorcontrib>Shah, Bhavin</creatorcontrib><creatorcontrib>Panopoulos, Athanasia D</creatorcontrib><creatorcontrib>Schluns, Kimberly S</creatorcontrib><creatorcontrib>Watowich, Stephanie S</creatorcontrib><creatorcontrib>Tian, Qiang</creatorcontrib><creatorcontrib>Jetten, Anton M</creatorcontrib><creatorcontrib>Dong, Chen</creatorcontrib><title>T Helper 17 Lineage Differentiation Is Programmed by Orphan Nuclear Receptors ROR[alpha] and ROR[gamma]</title><title>Immunity (Cambridge, Mass.)</title><description>T cell functional differentiation is mediated by lineage-specific transcription factors. T helper 17 (Th17) has been recently identified as a distinct Th lineage mediating tissue inflammation. Retinoic acid receptor-related orphan receptor γ (RORγ) was shown to regulate Th17 differentiation; RORγ deficiency, however, did not completely abolish Th17 cytokine expression. Here, we report Th17 cells highly expressed another related nuclear receptor, RORα, induced by transforming growth factor-β and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3. Overexpression of RORα promoted Th17 differentiation, possibly through the conserved noncoding sequence 2 inIl17-Il17flocus. RORα deficiency resulted in reduced IL-17 expressionin vitroandin vivo. Furthermore, RORα and RORγ coexpression synergistically led to greater Th17 differentiation. Double deficiencies in RORα and RORγ globally impaired Th17 generation and completely protected mice against experimental autoimmune encephalomyelitis. Therefore, Th17 differentiation is directed by two lineage-specific nuclear receptors, RORα and RORγ.</description><subject>Cancer</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Gene expression</subject><subject>Lymphocytes</subject><subject>Medical research</subject><subject>Rodents</subject><subject>Transcription factors</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNqNi8tOwzAQRS0EEuXxByxGYh0z07oxWfNQkRBFUXeoqoZ2EhwldrCTBX9PQHwAq_s49yp1RagJKb9ptOu60Ts9R7SaSE_lkZoRFjYzdIvHP96azOa0OFVnKTWIZJYFzlS9gZW0vUQgC8_OC9cC966qJIofHA8ueHhK8BpDHbnr5ADvX7CO_Qd7eBn3rXCEUvbSDyEmKNflG7cT3AL7w2-spxdvL9RJxW2Syz89V9ePD5u7VdbH8DlKGnZNGKOf0I6WaOY5FmgW_1t9AxleTik</recordid><startdate>20080118</startdate><enddate>20080118</enddate><creator>Yang, Xuexian O</creator><creator>Pappu, Bhanu P</creator><creator>Nurieva, Roza</creator><creator>Akimzhanov, Askar</creator><creator>Kang, Hong Soon</creator><creator>Chung, Yeonseok</creator><creator>Ma, Li</creator><creator>Shah, Bhavin</creator><creator>Panopoulos, Athanasia D</creator><creator>Schluns, Kimberly S</creator><creator>Watowich, Stephanie S</creator><creator>Tian, Qiang</creator><creator>Jetten, Anton M</creator><creator>Dong, Chen</creator><general>Elsevier Limited</general><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20080118</creationdate><title>T Helper 17 Lineage Differentiation Is Programmed by Orphan Nuclear Receptors ROR[alpha] and ROR[gamma]</title><author>Yang, Xuexian O ; 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T helper 17 (Th17) has been recently identified as a distinct Th lineage mediating tissue inflammation. Retinoic acid receptor-related orphan receptor γ (RORγ) was shown to regulate Th17 differentiation; RORγ deficiency, however, did not completely abolish Th17 cytokine expression. Here, we report Th17 cells highly expressed another related nuclear receptor, RORα, induced by transforming growth factor-β and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3. Overexpression of RORα promoted Th17 differentiation, possibly through the conserved noncoding sequence 2 inIl17-Il17flocus. RORα deficiency resulted in reduced IL-17 expressionin vitroandin vivo. Furthermore, RORα and RORγ coexpression synergistically led to greater Th17 differentiation. Double deficiencies in RORα and RORγ globally impaired Th17 generation and completely protected mice against experimental autoimmune encephalomyelitis. Therefore, Th17 differentiation is directed by two lineage-specific nuclear receptors, RORα and RORγ.</abstract><cop>Cambridge</cop><pub>Elsevier Limited</pub><doi>10.1016/j.immuni.2007.11.016</doi></addata></record> |
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| source | Elsevier ScienceDirect Journals Complete; Cell Press Free Archives; EZB-FREE-00999 freely available EZB journals |
| subjects | Cancer Deoxyribonucleic acid DNA Gene expression Lymphocytes Medical research Rodents Transcription factors |
| title | T Helper 17 Lineage Differentiation Is Programmed by Orphan Nuclear Receptors ROR[alpha] and ROR[gamma] |
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