Peroxisome proliferator-activated receptor delta limits the expansion of pathogenic Th cells during central nervous system autoimmunity
Peroxisome proliferator-activated receptors (PPARs; PPAR-alpha, PPAR-delta, and PPAR-gamma) comprise a family of nuclear receptors that sense fatty acid levels and translate this information into altered gene transcription. Previously, it was reported that treatment of mice with a synthetic ligand a...
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| Veröffentlicht in: | The Journal of experimental medicine 2010-08, Vol.207 (8), p.1599-1608 |
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| creator | Dunn, Shannon E Bhat, Roopa Straus, Daniel S Sobel, Raymond A Axtell, Robert Johnson, Amanda Nguyen, Kim Mukundan, Lata Moshkova, Marina Dugas, Jason C Chawla, Ajay Steinman, Lawrence |
| description | Peroxisome proliferator-activated receptors (PPARs; PPAR-alpha, PPAR-delta, and PPAR-gamma) comprise a family of nuclear receptors that sense fatty acid levels and translate this information into altered gene transcription. Previously, it was reported that treatment of mice with a synthetic ligand activator of PPAR-delta, GW0742, ameliorates experimental autoimmune encephalomyelitis (EAE), indicating a possible role for this nuclear receptor in the control of central nervous system (CNS) autoimmune inflammation. We show that mice deficient in PPAR-delta (PPAR-delta(-/-)) develop a severe inflammatory response during EAE characterized by a striking accumulation of IFN-gamma(+)IL-17A(-) and IFN-gamma(+)IL-17A(+) CD4(+) cells in the spinal cord. The preferential expansion of these T helper subsets in the CNS of PPAR-delta(-/-) mice occurred as a result of a constellation of immune system aberrations that included higher CD4(+) cell proliferation, cytokine production, and T-bet expression and enhanced expression of IL-12 family cytokines by myeloid cells. We also show that the effect of PPAR-delta in inhibiting the production of IFN-gamma and IL-12 family cytokines is ligand dependent and is observed in both mouse and human immune cells. Collectively, these findings suggest that PPAR-delta serves as an important molecular brake for the control of autoimmune inflammation. |
| doi_str_mv | 10.1084/jem.20091663 |
| format | Article |
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Previously, it was reported that treatment of mice with a synthetic ligand activator of PPAR-delta, GW0742, ameliorates experimental autoimmune encephalomyelitis (EAE), indicating a possible role for this nuclear receptor in the control of central nervous system (CNS) autoimmune inflammation. We show that mice deficient in PPAR-delta (PPAR-delta(-/-)) develop a severe inflammatory response during EAE characterized by a striking accumulation of IFN-gamma(+)IL-17A(-) and IFN-gamma(+)IL-17A(+) CD4(+) cells in the spinal cord. The preferential expansion of these T helper subsets in the CNS of PPAR-delta(-/-) mice occurred as a result of a constellation of immune system aberrations that included higher CD4(+) cell proliferation, cytokine production, and T-bet expression and enhanced expression of IL-12 family cytokines by myeloid cells. We also show that the effect of PPAR-delta in inhibiting the production of IFN-gamma and IL-12 family cytokines is ligand dependent and is observed in both mouse and human immune cells. Collectively, these findings suggest that PPAR-delta serves as an important molecular brake for the control of autoimmune inflammation.</description><identifier>ISSN: 0022-1007</identifier><identifier>EISSN: 1540-9538</identifier><identifier>DOI: 10.1084/jem.20091663</identifier><identifier>PMID: 20624891</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>Animals ; Brain - immunology ; Brain - pathology ; Brief Definitive Report ; CD4-Positive T-Lymphocytes - drug effects ; CD4-Positive T-Lymphocytes - immunology ; CD4-Positive T-Lymphocytes - metabolism ; CD4-Positive T-Lymphocytes - transplantation ; Cell Proliferation ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - metabolism ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Female ; Gene Expression - immunology ; Glycoproteins - immunology ; Homeodomain Proteins - genetics ; Humans ; Interferon-gamma - genetics ; Interferon-gamma - metabolism ; Interleukin-12 - genetics ; Interleukin-12 - metabolism ; Interleukin-17 - genetics ; Interleukin-17 - metabolism ; Leukocytes, Mononuclear - drug effects ; Leukocytes, Mononuclear - immunology ; Leukocytes, Mononuclear - metabolism ; Lipopolysaccharides - pharmacology ; Lymphocyte Activation - immunology ; Macrophages, Peritoneal - drug effects ; Macrophages, Peritoneal - immunology ; Macrophages, Peritoneal - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelin-Oligodendrocyte Glycoprotein ; Myeloid Cells - drug effects ; Myeloid Cells - immunology ; Myeloid Cells - metabolism ; Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics ; Peptide Fragments - immunology ; PPAR delta - antagonists & inhibitors ; PPAR delta - metabolism ; Spinal Cord - immunology ; Spinal Cord - pathology ; T-Box Domain Proteins - genetics ; T-Lymphocytes, Helper-Inducer - drug effects ; T-Lymphocytes, Helper-Inducer - immunology ; T-Lymphocytes, Helper-Inducer - pathology ; T-Lymphocytes, Helper-Inducer - transplantation ; Th1 Cells - immunology ; Th1 Cells - metabolism ; Thiazoles - pharmacology ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>The Journal of experimental medicine, 2010-08, Vol.207 (8), p.1599-1608</ispartof><rights>2010 Dunn et al. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c383t-37f2de1d92550e438573f7a3a414b80438eec7766da7e1586b8dfbbd0f2c31203</citedby><cites>FETCH-LOGICAL-c383t-37f2de1d92550e438573f7a3a414b80438eec7766da7e1586b8dfbbd0f2c31203</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20624891$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dunn, Shannon E</creatorcontrib><creatorcontrib>Bhat, Roopa</creatorcontrib><creatorcontrib>Straus, Daniel S</creatorcontrib><creatorcontrib>Sobel, Raymond A</creatorcontrib><creatorcontrib>Axtell, Robert</creatorcontrib><creatorcontrib>Johnson, Amanda</creatorcontrib><creatorcontrib>Nguyen, Kim</creatorcontrib><creatorcontrib>Mukundan, Lata</creatorcontrib><creatorcontrib>Moshkova, Marina</creatorcontrib><creatorcontrib>Dugas, Jason C</creatorcontrib><creatorcontrib>Chawla, Ajay</creatorcontrib><creatorcontrib>Steinman, Lawrence</creatorcontrib><title>Peroxisome proliferator-activated receptor delta limits the expansion of pathogenic Th cells during central nervous system autoimmunity</title><title>The Journal of experimental medicine</title><addtitle>J Exp Med</addtitle><description>Peroxisome proliferator-activated receptors (PPARs; PPAR-alpha, PPAR-delta, and PPAR-gamma) comprise a family of nuclear receptors that sense fatty acid levels and translate this information into altered gene transcription. Previously, it was reported that treatment of mice with a synthetic ligand activator of PPAR-delta, GW0742, ameliorates experimental autoimmune encephalomyelitis (EAE), indicating a possible role for this nuclear receptor in the control of central nervous system (CNS) autoimmune inflammation. We show that mice deficient in PPAR-delta (PPAR-delta(-/-)) develop a severe inflammatory response during EAE characterized by a striking accumulation of IFN-gamma(+)IL-17A(-) and IFN-gamma(+)IL-17A(+) CD4(+) cells in the spinal cord. The preferential expansion of these T helper subsets in the CNS of PPAR-delta(-/-) mice occurred as a result of a constellation of immune system aberrations that included higher CD4(+) cell proliferation, cytokine production, and T-bet expression and enhanced expression of IL-12 family cytokines by myeloid cells. We also show that the effect of PPAR-delta in inhibiting the production of IFN-gamma and IL-12 family cytokines is ligand dependent and is observed in both mouse and human immune cells. Collectively, these findings suggest that PPAR-delta serves as an important molecular brake for the control of autoimmune inflammation.</description><subject>Animals</subject><subject>Brain - immunology</subject><subject>Brain - pathology</subject><subject>Brief Definitive Report</subject><subject>CD4-Positive T-Lymphocytes - drug effects</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>CD4-Positive T-Lymphocytes - transplantation</subject><subject>Cell Proliferation</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - metabolism</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Female</subject><subject>Gene Expression - immunology</subject><subject>Glycoproteins - immunology</subject><subject>Homeodomain Proteins - genetics</subject><subject>Humans</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-12 - genetics</subject><subject>Interleukin-12 - metabolism</subject><subject>Interleukin-17 - genetics</subject><subject>Interleukin-17 - metabolism</subject><subject>Leukocytes, Mononuclear - drug effects</subject><subject>Leukocytes, Mononuclear - immunology</subject><subject>Leukocytes, Mononuclear - metabolism</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Lymphocyte Activation - immunology</subject><subject>Macrophages, Peritoneal - drug effects</subject><subject>Macrophages, Peritoneal - immunology</subject><subject>Macrophages, Peritoneal - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Myelin-Oligodendrocyte Glycoprotein</subject><subject>Myeloid Cells - drug effects</subject><subject>Myeloid Cells - immunology</subject><subject>Myeloid Cells - metabolism</subject><subject>Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics</subject><subject>Peptide Fragments - immunology</subject><subject>PPAR delta - antagonists & inhibitors</subject><subject>PPAR delta - metabolism</subject><subject>Spinal Cord - immunology</subject><subject>Spinal Cord - pathology</subject><subject>T-Box Domain Proteins - genetics</subject><subject>T-Lymphocytes, Helper-Inducer - drug effects</subject><subject>T-Lymphocytes, Helper-Inducer - immunology</subject><subject>T-Lymphocytes, Helper-Inducer - pathology</subject><subject>T-Lymphocytes, Helper-Inducer - transplantation</subject><subject>Th1 Cells - immunology</subject><subject>Th1 Cells - metabolism</subject><subject>Thiazoles - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0022-1007</issn><issn>1540-9538</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1v1DAQtRCILoUbZ-QbF1LGH4m9FyRUlQ-pEhzK2XLiya6rOA62s-r-Av42rrqt4DSaN09vZt4j5C2DCwZafrzFcMEBtqzrxDOyYa2EZtsK_ZxsADhvGIA6I69yvgVgUrbdS3LGoeNSb9mG_PmJKd75HAPSJcXJj5hsiamxQ_EHW9DRhAMuFaIOp2Lp5IMvmZY9Urxb7Jx9nGkc6WLLPu5w9gO92dMBpylTtyY_72ozl2QnOmM6xDXTfMwFA7VriT6Edfbl-Jq8GO2U8c2pnpNfX65uLr811z--fr_8fN0MQovSCDVyh8xtedsCSqFbJUZlhZVM9hoqgDgo1XXOKmSt7nrtxr53MPJBMA7inHx60F3WPqA7XWaW5INNRxOtN_9PZr83u3gwvBrMuKoC708CKf5eMRcTfL7_1s5YfzOq-ipBt7wyPzwwhxRzTjg-bWFg7qMzNTrzGF2lv_v3sifyY1biL0b1mgg</recordid><startdate>20100802</startdate><enddate>20100802</enddate><creator>Dunn, Shannon E</creator><creator>Bhat, Roopa</creator><creator>Straus, Daniel S</creator><creator>Sobel, Raymond A</creator><creator>Axtell, Robert</creator><creator>Johnson, Amanda</creator><creator>Nguyen, Kim</creator><creator>Mukundan, Lata</creator><creator>Moshkova, Marina</creator><creator>Dugas, Jason C</creator><creator>Chawla, Ajay</creator><creator>Steinman, Lawrence</creator><general>The Rockefeller University Press</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100802</creationdate><title>Peroxisome proliferator-activated receptor delta limits the expansion of pathogenic Th cells during central nervous system autoimmunity</title><author>Dunn, Shannon E ; Bhat, Roopa ; Straus, Daniel S ; Sobel, Raymond A ; Axtell, Robert ; Johnson, Amanda ; Nguyen, Kim ; Mukundan, Lata ; Moshkova, Marina ; Dugas, Jason C ; Chawla, Ajay ; Steinman, Lawrence</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c383t-37f2de1d92550e438573f7a3a414b80438eec7766da7e1586b8dfbbd0f2c31203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Brain - immunology</topic><topic>Brain - pathology</topic><topic>Brief Definitive Report</topic><topic>CD4-Positive T-Lymphocytes - drug effects</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>CD4-Positive T-Lymphocytes - transplantation</topic><topic>Cell Proliferation</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - metabolism</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Female</topic><topic>Gene Expression - immunology</topic><topic>Glycoproteins - immunology</topic><topic>Homeodomain Proteins - genetics</topic><topic>Humans</topic><topic>Interferon-gamma - genetics</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-12 - genetics</topic><topic>Interleukin-12 - metabolism</topic><topic>Interleukin-17 - genetics</topic><topic>Interleukin-17 - metabolism</topic><topic>Leukocytes, Mononuclear - drug effects</topic><topic>Leukocytes, Mononuclear - immunology</topic><topic>Leukocytes, Mononuclear - metabolism</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Lymphocyte Activation - immunology</topic><topic>Macrophages, Peritoneal - drug effects</topic><topic>Macrophages, Peritoneal - immunology</topic><topic>Macrophages, Peritoneal - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Myelin-Oligodendrocyte Glycoprotein</topic><topic>Myeloid Cells - drug effects</topic><topic>Myeloid Cells - immunology</topic><topic>Myeloid Cells - metabolism</topic><topic>Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics</topic><topic>Peptide Fragments - immunology</topic><topic>PPAR delta - antagonists & inhibitors</topic><topic>PPAR delta - metabolism</topic><topic>Spinal Cord - immunology</topic><topic>Spinal Cord - pathology</topic><topic>T-Box Domain Proteins - genetics</topic><topic>T-Lymphocytes, Helper-Inducer - drug effects</topic><topic>T-Lymphocytes, Helper-Inducer - immunology</topic><topic>T-Lymphocytes, Helper-Inducer - pathology</topic><topic>T-Lymphocytes, Helper-Inducer - transplantation</topic><topic>Th1 Cells - immunology</topic><topic>Th1 Cells - metabolism</topic><topic>Thiazoles - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dunn, Shannon E</creatorcontrib><creatorcontrib>Bhat, Roopa</creatorcontrib><creatorcontrib>Straus, Daniel S</creatorcontrib><creatorcontrib>Sobel, Raymond A</creatorcontrib><creatorcontrib>Axtell, Robert</creatorcontrib><creatorcontrib>Johnson, Amanda</creatorcontrib><creatorcontrib>Nguyen, Kim</creatorcontrib><creatorcontrib>Mukundan, Lata</creatorcontrib><creatorcontrib>Moshkova, Marina</creatorcontrib><creatorcontrib>Dugas, Jason C</creatorcontrib><creatorcontrib>Chawla, Ajay</creatorcontrib><creatorcontrib>Steinman, Lawrence</creatorcontrib><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>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dunn, Shannon E</au><au>Bhat, Roopa</au><au>Straus, Daniel S</au><au>Sobel, Raymond A</au><au>Axtell, Robert</au><au>Johnson, Amanda</au><au>Nguyen, Kim</au><au>Mukundan, Lata</au><au>Moshkova, Marina</au><au>Dugas, Jason C</au><au>Chawla, Ajay</au><au>Steinman, Lawrence</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peroxisome proliferator-activated receptor delta limits the expansion of pathogenic Th cells during central nervous system autoimmunity</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>2010-08-02</date><risdate>2010</risdate><volume>207</volume><issue>8</issue><spage>1599</spage><epage>1608</epage><pages>1599-1608</pages><issn>0022-1007</issn><eissn>1540-9538</eissn><abstract>Peroxisome proliferator-activated receptors (PPARs; PPAR-alpha, PPAR-delta, and PPAR-gamma) comprise a family of nuclear receptors that sense fatty acid levels and translate this information into altered gene transcription. Previously, it was reported that treatment of mice with a synthetic ligand activator of PPAR-delta, GW0742, ameliorates experimental autoimmune encephalomyelitis (EAE), indicating a possible role for this nuclear receptor in the control of central nervous system (CNS) autoimmune inflammation. We show that mice deficient in PPAR-delta (PPAR-delta(-/-)) develop a severe inflammatory response during EAE characterized by a striking accumulation of IFN-gamma(+)IL-17A(-) and IFN-gamma(+)IL-17A(+) CD4(+) cells in the spinal cord. The preferential expansion of these T helper subsets in the CNS of PPAR-delta(-/-) mice occurred as a result of a constellation of immune system aberrations that included higher CD4(+) cell proliferation, cytokine production, and T-bet expression and enhanced expression of IL-12 family cytokines by myeloid cells. We also show that the effect of PPAR-delta in inhibiting the production of IFN-gamma and IL-12 family cytokines is ligand dependent and is observed in both mouse and human immune cells. Collectively, these findings suggest that PPAR-delta serves as an important molecular brake for the control of autoimmune inflammation.</abstract><cop>United States</cop><pub>The Rockefeller University Press</pub><pmid>20624891</pmid><doi>10.1084/jem.20091663</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Brain - immunology Brain - pathology Brief Definitive Report CD4-Positive T-Lymphocytes - drug effects CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - metabolism CD4-Positive T-Lymphocytes - transplantation Cell Proliferation Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Female Gene Expression - immunology Glycoproteins - immunology Homeodomain Proteins - genetics Humans Interferon-gamma - genetics Interferon-gamma - metabolism Interleukin-12 - genetics Interleukin-12 - metabolism Interleukin-17 - genetics Interleukin-17 - metabolism Leukocytes, Mononuclear - drug effects Leukocytes, Mononuclear - immunology Leukocytes, Mononuclear - metabolism Lipopolysaccharides - pharmacology Lymphocyte Activation - immunology Macrophages, Peritoneal - drug effects Macrophages, Peritoneal - immunology Macrophages, Peritoneal - metabolism Male Mice Mice, Inbred C57BL Mice, Knockout Myelin-Oligodendrocyte Glycoprotein Myeloid Cells - drug effects Myeloid Cells - immunology Myeloid Cells - metabolism Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics Peptide Fragments - immunology PPAR delta - antagonists & inhibitors PPAR delta - metabolism Spinal Cord - immunology Spinal Cord - pathology T-Box Domain Proteins - genetics T-Lymphocytes, Helper-Inducer - drug effects T-Lymphocytes, Helper-Inducer - immunology T-Lymphocytes, Helper-Inducer - pathology T-Lymphocytes, Helper-Inducer - transplantation Th1 Cells - immunology Th1 Cells - metabolism Thiazoles - pharmacology Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism |
| title | Peroxisome proliferator-activated receptor delta limits the expansion of pathogenic Th cells during central nervous system autoimmunity |
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