Critical role of all-trans retinoic acid in stabilizing human natural regulatory T cells under inflammatory conditions
Recent studies have demonstrated that thymus-derived naturally occurring CD4 ⁺Foxp3 ⁺ regulatory T cells (Tregs) in human and mouse may be unstable and dysfunctional in the presence of proinflammatory cytokines. All - trans RA (atRA), the active derivative of vitamin A, has been shown to regulate Tr...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2014-08, Vol.111 (33), p.E3432-E3440 |
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| creator | Lu, Ling Lan, Qin Li, Zhiyuan Zhou, Xiaohui Gu, Jian Li, Qiang Wang, Julie Chen, Maogen Liu, Ya Shen, Yi Brand, David D Ryffel, Bernhard Horwitz, David A Quismorio, Francisco P Liu, Zhongmin Li, Bin Olsen, Nancy J Zheng, Song Guo |
| description | Recent studies have demonstrated that thymus-derived naturally occurring CD4 ⁺Foxp3 ⁺ regulatory T cells (Tregs) in human and mouse may be unstable and dysfunctional in the presence of proinflammatory cytokines. All - trans RA (atRA), the active derivative of vitamin A, has been shown to regulate Treg and T effector cell differentiation. We hypothesize atRA stabilizes human natural Tregs (nTregs) under inflammatory conditions. atRA prevents human nTregs from converting to Th1 and/or Th17 cells and sustains their Foxp3 expression and suppressive function in vitro or in vivo following encounters with IL-1 and IL-6. Interestingly, adoptive transfer of human nTregs pretreated with atRA significantly enhanced their suppressive effects on xenograft-vs.-host diseases (xGVHDs), and atRA- but not rapamycin-pretreated nTregs sustained the functional activity against xGVHD after stimulation with IL-1/IL-6. atRA suppresses IL-1 receptor (IL-1R) up-regulation, accelerates IL-6R down-regulation, and diminishes their signaling events as well as prevents the up-regulation of STIP1 homology and U-Box containing protein 1 on Foxp3 ⁺ cells following IL-1/IL-6 stimulation. atRA also increases histone acetylation on Foxp3 gene promoter and CpG demethylation in the region of Foxp3 locus (i.e., Treg-specific demethylated region). These results strongly implicate that nTregs primed with atRA may represent a novel treatment strategy to control established chronic immune-mediated autoimmune and inflammatory diseases. |
| doi_str_mv | 10.1073/pnas.1408780111 |
| format | Article |
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All - trans RA (atRA), the active derivative of vitamin A, has been shown to regulate Treg and T effector cell differentiation. We hypothesize atRA stabilizes human natural Tregs (nTregs) under inflammatory conditions. atRA prevents human nTregs from converting to Th1 and/or Th17 cells and sustains their Foxp3 expression and suppressive function in vitro or in vivo following encounters with IL-1 and IL-6. Interestingly, adoptive transfer of human nTregs pretreated with atRA significantly enhanced their suppressive effects on xenograft-vs.-host diseases (xGVHDs), and atRA- but not rapamycin-pretreated nTregs sustained the functional activity against xGVHD after stimulation with IL-1/IL-6. atRA suppresses IL-1 receptor (IL-1R) up-regulation, accelerates IL-6R down-regulation, and diminishes their signaling events as well as prevents the up-regulation of STIP1 homology and U-Box containing protein 1 on Foxp3 ⁺ cells following IL-1/IL-6 stimulation. atRA also increases histone acetylation on Foxp3 gene promoter and CpG demethylation in the region of Foxp3 locus (i.e., Treg-specific demethylated region). These results strongly implicate that nTregs primed with atRA may represent a novel treatment strategy to control established chronic immune-mediated autoimmune and inflammatory diseases.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1408780111</identifier><identifier>PMID: 25099355</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Base Sequence ; Biological Sciences ; Cellular biology ; Cytokines - physiology ; DNA Primers ; Epigenetics ; Flow Cytometry ; Forkhead Transcription Factors - metabolism ; Gene expression ; Humans ; Inflammation - immunology ; Inflammation - pathology ; Inflammatory diseases ; Interleukin-1 - physiology ; Interleukin-6 - physiology ; PNAS Plus ; Real-Time Polymerase Chain Reaction ; Receptors, Interleukin-1 - metabolism ; Receptors, Interleukin-6 - metabolism ; T-Lymphocytes, Regulatory - drug effects ; T-Lymphocytes, Regulatory - immunology ; Tretinoin - pharmacology ; Ubiquitin-Protein Ligases - metabolism</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2014-08, Vol.111 (33), p.E3432-E3440</ispartof><rights>Copyright National Academy of Sciences Aug 19, 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-248c4522117bd1c12516b8eed5239a2a8b96bb6eb380209a3a832be9f6058f143</citedby><cites>FETCH-LOGICAL-c503t-248c4522117bd1c12516b8eed5239a2a8b96bb6eb380209a3a832be9f6058f143</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/111/33.cover.gif</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143025/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143025/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25099355$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Ling</creatorcontrib><creatorcontrib>Lan, Qin</creatorcontrib><creatorcontrib>Li, Zhiyuan</creatorcontrib><creatorcontrib>Zhou, Xiaohui</creatorcontrib><creatorcontrib>Gu, Jian</creatorcontrib><creatorcontrib>Li, Qiang</creatorcontrib><creatorcontrib>Wang, Julie</creatorcontrib><creatorcontrib>Chen, Maogen</creatorcontrib><creatorcontrib>Liu, Ya</creatorcontrib><creatorcontrib>Shen, Yi</creatorcontrib><creatorcontrib>Brand, David D</creatorcontrib><creatorcontrib>Ryffel, Bernhard</creatorcontrib><creatorcontrib>Horwitz, David A</creatorcontrib><creatorcontrib>Quismorio, Francisco P</creatorcontrib><creatorcontrib>Liu, Zhongmin</creatorcontrib><creatorcontrib>Li, Bin</creatorcontrib><creatorcontrib>Olsen, Nancy J</creatorcontrib><creatorcontrib>Zheng, Song Guo</creatorcontrib><title>Critical role of all-trans retinoic acid in stabilizing human natural regulatory T cells under inflammatory conditions</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Recent studies have demonstrated that thymus-derived naturally occurring CD4 ⁺Foxp3 ⁺ regulatory T cells (Tregs) in human and mouse may be unstable and dysfunctional in the presence of proinflammatory cytokines. All - trans RA (atRA), the active derivative of vitamin A, has been shown to regulate Treg and T effector cell differentiation. We hypothesize atRA stabilizes human natural Tregs (nTregs) under inflammatory conditions. atRA prevents human nTregs from converting to Th1 and/or Th17 cells and sustains their Foxp3 expression and suppressive function in vitro or in vivo following encounters with IL-1 and IL-6. Interestingly, adoptive transfer of human nTregs pretreated with atRA significantly enhanced their suppressive effects on xenograft-vs.-host diseases (xGVHDs), and atRA- but not rapamycin-pretreated nTregs sustained the functional activity against xGVHD after stimulation with IL-1/IL-6. atRA suppresses IL-1 receptor (IL-1R) up-regulation, accelerates IL-6R down-regulation, and diminishes their signaling events as well as prevents the up-regulation of STIP1 homology and U-Box containing protein 1 on Foxp3 ⁺ cells following IL-1/IL-6 stimulation. atRA also increases histone acetylation on Foxp3 gene promoter and CpG demethylation in the region of Foxp3 locus (i.e., Treg-specific demethylated region). These results strongly implicate that nTregs primed with atRA may represent a novel treatment strategy to control established chronic immune-mediated autoimmune and inflammatory diseases.</description><subject>Base Sequence</subject><subject>Biological Sciences</subject><subject>Cellular biology</subject><subject>Cytokines - physiology</subject><subject>DNA Primers</subject><subject>Epigenetics</subject><subject>Flow Cytometry</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Inflammation - immunology</subject><subject>Inflammation - pathology</subject><subject>Inflammatory diseases</subject><subject>Interleukin-1 - physiology</subject><subject>Interleukin-6 - physiology</subject><subject>PNAS Plus</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Receptors, Interleukin-1 - metabolism</subject><subject>Receptors, Interleukin-6 - metabolism</subject><subject>T-Lymphocytes, Regulatory - drug effects</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Tretinoin - pharmacology</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1v1DAQxSMEokvhzA0sceGSdsYfWfuCVK1KQarEgfZsOYmzdeXYi51UKn89jnbZAidOPszvPb83U1VvEc4Q1ux8F0w-Qw5yLQERn1UrBIV1wxU8r1YAdF1LTvlJ9SrnewBQQsLL6oQKUIoJsaoeNslNrjOepOgtiQMx3tdTMiGTZCcXouuI6VxPXCB5Mq3z7qcLW3I3jyaQYKY5LWK7nb2ZYnokN6Sz3mcyh96mohq8Gcf9qIuhL7_FkF9XLwbjs31zeE-r28-XN5sv9fW3q6-bi-u6E8CmmnLZcUEp4rrtsUMqsGmltb2gTBlqZKuatm1syyRQUIYZyWhr1dCAkANydlp92vvu5na0fWdDqeb1LrnRpEcdjdN_T4K709v4oHkRAxXF4OPBIMUfs82THl1eCppg45w1iqaRQiKT_4EKUQqBogX98A96H-cUyiYWqgFoBK4Ldb6nuhRzTnY45kbQy_n1cn79dP6iePdn3SP_-94FIAdgUR7tEDVj-pJxtmR7v0cGE7XZJpf17XcKWFKVnfCS6xdj9MCK</recordid><startdate>20140819</startdate><enddate>20140819</enddate><creator>Lu, Ling</creator><creator>Lan, Qin</creator><creator>Li, Zhiyuan</creator><creator>Zhou, Xiaohui</creator><creator>Gu, Jian</creator><creator>Li, Qiang</creator><creator>Wang, Julie</creator><creator>Chen, Maogen</creator><creator>Liu, Ya</creator><creator>Shen, Yi</creator><creator>Brand, David D</creator><creator>Ryffel, Bernhard</creator><creator>Horwitz, David A</creator><creator>Quismorio, Francisco P</creator><creator>Liu, Zhongmin</creator><creator>Li, Bin</creator><creator>Olsen, Nancy J</creator><creator>Zheng, Song Guo</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>FBQ</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140819</creationdate><title>Critical role of all-trans retinoic acid in stabilizing human natural regulatory T cells under inflammatory conditions</title><author>Lu, Ling ; 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All - trans RA (atRA), the active derivative of vitamin A, has been shown to regulate Treg and T effector cell differentiation. We hypothesize atRA stabilizes human natural Tregs (nTregs) under inflammatory conditions. atRA prevents human nTregs from converting to Th1 and/or Th17 cells and sustains their Foxp3 expression and suppressive function in vitro or in vivo following encounters with IL-1 and IL-6. Interestingly, adoptive transfer of human nTregs pretreated with atRA significantly enhanced their suppressive effects on xenograft-vs.-host diseases (xGVHDs), and atRA- but not rapamycin-pretreated nTregs sustained the functional activity against xGVHD after stimulation with IL-1/IL-6. atRA suppresses IL-1 receptor (IL-1R) up-regulation, accelerates IL-6R down-regulation, and diminishes their signaling events as well as prevents the up-regulation of STIP1 homology and U-Box containing protein 1 on Foxp3 ⁺ cells following IL-1/IL-6 stimulation. atRA also increases histone acetylation on Foxp3 gene promoter and CpG demethylation in the region of Foxp3 locus (i.e., Treg-specific demethylated region). These results strongly implicate that nTregs primed with atRA may represent a novel treatment strategy to control established chronic immune-mediated autoimmune and inflammatory diseases.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>25099355</pmid><doi>10.1073/pnas.1408780111</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Base Sequence Biological Sciences Cellular biology Cytokines - physiology DNA Primers Epigenetics Flow Cytometry Forkhead Transcription Factors - metabolism Gene expression Humans Inflammation - immunology Inflammation - pathology Inflammatory diseases Interleukin-1 - physiology Interleukin-6 - physiology PNAS Plus Real-Time Polymerase Chain Reaction Receptors, Interleukin-1 - metabolism Receptors, Interleukin-6 - metabolism T-Lymphocytes, Regulatory - drug effects T-Lymphocytes, Regulatory - immunology Tretinoin - pharmacology Ubiquitin-Protein Ligases - metabolism |
| title | Critical role of all-trans retinoic acid in stabilizing human natural regulatory T cells under inflammatory conditions |
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