A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells
Experimental autoimmune encephalomyelitis (EAE) is a prototype autoimmune disease mediated by type 1 helper T (T H 1) cells and under the control of regulatory cells 1 , 2 , 3 . Here we report that a synthetic glycolipid ligand for CD1d-restricted natural killer T (NKT) cells expressing the semi-inv...
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| Veröffentlicht in: | Nature (London) 2001-10, Vol.413 (6855), p.531-534 |
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| creator | Miyamoto, Katsuichi Miyake, Sachiko Yamamura, Takashi |
| description | Experimental autoimmune encephalomyelitis (EAE) is a prototype autoimmune disease mediated by type 1 helper T (T
H
1) cells and under the control of regulatory cells
1
,
2
,
3
. Here we report that a synthetic glycolipid ligand for CD1d-restricted natural killer T (NKT) cells expressing the semi-invariant T-cell receptor (Vα14
+
) is preventive against EAE. The ligand is an analogue of α-galactosylceramide (α-GC), a prototype NKT cell ligand, with a truncated sphingosine chain. α-GC causes NKT cells to produce both interferon (IFN)-γ and interleukin (IL)-4 (refs
4
,
5
). However, this new ligand can induce a predominant production of IL-4 by the NKT cells. A single injection of this glycolipid, but not of α-GC, consistently induced T
H
2 bias of autoimmune T cells by causing NKT cells to produce IL-4, leading to suppression of EAE. The lack of polymorphism of CD1d and cross-reactive response of mouse and human NKT cells to the same ligand
6
indicates that targeting NKT cells with this ligand may be an attractive means for intervening in human autoimmune diseases such as multiple sclerosis. |
| doi_str_mv | 10.1038/35097097 |
| format | Article |
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H
1) cells and under the control of regulatory cells
1
,
2
,
3
. Here we report that a synthetic glycolipid ligand for CD1d-restricted natural killer T (NKT) cells expressing the semi-invariant T-cell receptor (Vα14
+
) is preventive against EAE. The ligand is an analogue of α-galactosylceramide (α-GC), a prototype NKT cell ligand, with a truncated sphingosine chain. α-GC causes NKT cells to produce both interferon (IFN)-γ and interleukin (IL)-4 (refs
4
,
5
). However, this new ligand can induce a predominant production of IL-4 by the NKT cells. A single injection of this glycolipid, but not of α-GC, consistently induced T
H
2 bias of autoimmune T cells by causing NKT cells to produce IL-4, leading to suppression of EAE. The lack of polymorphism of CD1d and cross-reactive response of mouse and human NKT cells to the same ligand
6
indicates that targeting NKT cells with this ligand may be an attractive means for intervening in human autoimmune diseases such as multiple sclerosis.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/35097097</identifier><identifier>PMID: 11586362</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Amino Acid Sequence ; Animals ; Antigens, CD1 - immunology ; Antigens, CD1d ; Biological and medical sciences ; Encephalomyelitis, Autoimmune, Experimental - prevention & control ; Fundamental and applied biological sciences. Psychology ; Galactosylceramides - chemistry ; Glycolipids - chemistry ; Glycolipids - therapeutic use ; Humanities and Social Sciences ; Immunoglobulin G - immunology ; Interferon-gamma - biosynthesis ; Interferon-gamma - blood ; Interleukin-4 - biosynthesis ; Interleukin-4 - blood ; Killer Cells, Natural - immunology ; letter ; Ligands ; Lymphocyte Subsets - immunology ; Mice ; Molecular and cellular biology ; Molecular Sequence Data ; multidisciplinary ; Science ; Science (multidisciplinary) ; Th2 Cells - immunology</subject><ispartof>Nature (London), 2001-10, Vol.413 (6855), p.531-534</ispartof><rights>Macmillan Magazines Ltd. 2001</rights><rights>2002 INIST-CNRS</rights><rights>COPYRIGHT 2001 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3967-c3f3f15b4a7965213f3715c44f809f3fe2650c7f29f6b22ef8685029e8a0cf2e3</citedby><cites>FETCH-LOGICAL-c3967-c3f3f15b4a7965213f3715c44f809f3fe2650c7f29f6b22ef8685029e8a0cf2e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/35097097$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/35097097$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14159002$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11586362$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miyamoto, Katsuichi</creatorcontrib><creatorcontrib>Miyake, Sachiko</creatorcontrib><creatorcontrib>Yamamura, Takashi</creatorcontrib><title>A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells</title><title>Nature (London)</title><addtitle>Nature</addtitle><addtitle>Nature</addtitle><description>Experimental autoimmune encephalomyelitis (EAE) is a prototype autoimmune disease mediated by type 1 helper T (T
H
1) cells and under the control of regulatory cells
1
,
2
,
3
. Here we report that a synthetic glycolipid ligand for CD1d-restricted natural killer T (NKT) cells expressing the semi-invariant T-cell receptor (Vα14
+
) is preventive against EAE. The ligand is an analogue of α-galactosylceramide (α-GC), a prototype NKT cell ligand, with a truncated sphingosine chain. α-GC causes NKT cells to produce both interferon (IFN)-γ and interleukin (IL)-4 (refs
4
,
5
). However, this new ligand can induce a predominant production of IL-4 by the NKT cells. A single injection of this glycolipid, but not of α-GC, consistently induced T
H
2 bias of autoimmune T cells by causing NKT cells to produce IL-4, leading to suppression of EAE. The lack of polymorphism of CD1d and cross-reactive response of mouse and human NKT cells to the same ligand
6
indicates that targeting NKT cells with this ligand may be an attractive means for intervening in human autoimmune diseases such as multiple sclerosis.</description><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Antigens, CD1 - immunology</subject><subject>Antigens, CD1d</subject><subject>Biological and medical sciences</subject><subject>Encephalomyelitis, Autoimmune, Experimental - prevention & control</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Galactosylceramides - chemistry</subject><subject>Glycolipids - chemistry</subject><subject>Glycolipids - therapeutic use</subject><subject>Humanities and Social Sciences</subject><subject>Immunoglobulin G - immunology</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Interferon-gamma - blood</subject><subject>Interleukin-4 - biosynthesis</subject><subject>Interleukin-4 - blood</subject><subject>Killer Cells, Natural - immunology</subject><subject>letter</subject><subject>Ligands</subject><subject>Lymphocyte Subsets - immunology</subject><subject>Mice</subject><subject>Molecular and cellular biology</subject><subject>Molecular Sequence Data</subject><subject>multidisciplinary</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Th2 Cells - immunology</subject><issn>0028-0836</issn><issn>1476-4687</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptktFqFDEUhoModq2CTyBBsOjF1CQzycxcLqXaQkHQ9XrIZE-maTPJNMmI8_am7MpaXBISkvOdk5-cH6G3lJxTUjafS07aOs9naEWrWhSVaOrnaEUIawrSlOIEvYrxjhDCaV29RCeU8kaUgq3Q_RrHxaVbSEbhwS7KWzOZLZ4C_AKXIpZz8mYcZwcYnILpVlo_LmBNMhH3CzZuOyvjBry5Yrg3MmKvsZNpDtLie2MtBLzBCqyNr9ELLW2EN_v9FP38crm5uCpuvn29vljfFKpsRZ1XXWrK-0rWreCM5mNNuaoq3ZA2h4AJTlStWatFzxjoRjScsBYaSZRmUJ6is13dKfiHGWLqRhMfFUgHfo5dTVnVVqTKYLEDB2mhM077FKQawEEW7x1ok6_XtMk6RM1p5t8f4dVkHrp_ofMjUB5bGI06WvXTk4TMJPidBjnH2F3_-P6U_bhjVfAxBtDdFMwow9JR0j1aoftrhYy-2__C3I-wPYD73mfgwx6QUUmrg3TKxANXUd5mBx30xRxyA4Tuzs_B5Q7-_-gfGhDFVA</recordid><startdate>20011004</startdate><enddate>20011004</enddate><creator>Miyamoto, Katsuichi</creator><creator>Miyake, Sachiko</creator><creator>Yamamura, Takashi</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</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></search><sort><creationdate>20011004</creationdate><title>A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells</title><author>Miyamoto, Katsuichi ; Miyake, Sachiko ; Yamamura, Takashi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3967-c3f3f15b4a7965213f3715c44f809f3fe2650c7f29f6b22ef8685029e8a0cf2e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Antigens, CD1 - immunology</topic><topic>Antigens, CD1d</topic><topic>Biological and medical sciences</topic><topic>Encephalomyelitis, Autoimmune, Experimental - prevention & control</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Galactosylceramides - chemistry</topic><topic>Glycolipids - chemistry</topic><topic>Glycolipids - therapeutic use</topic><topic>Humanities and Social Sciences</topic><topic>Immunoglobulin G - immunology</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Interferon-gamma - blood</topic><topic>Interleukin-4 - biosynthesis</topic><topic>Interleukin-4 - blood</topic><topic>Killer Cells, Natural - immunology</topic><topic>letter</topic><topic>Ligands</topic><topic>Lymphocyte Subsets - immunology</topic><topic>Mice</topic><topic>Molecular and cellular biology</topic><topic>Molecular Sequence Data</topic><topic>multidisciplinary</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Th2 Cells - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miyamoto, Katsuichi</creatorcontrib><creatorcontrib>Miyake, Sachiko</creatorcontrib><creatorcontrib>Yamamura, Takashi</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><jtitle>Nature (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miyamoto, Katsuichi</au><au>Miyake, Sachiko</au><au>Yamamura, Takashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells</atitle><jtitle>Nature (London)</jtitle><stitle>Nature</stitle><addtitle>Nature</addtitle><date>2001-10-04</date><risdate>2001</risdate><volume>413</volume><issue>6855</issue><spage>531</spage><epage>534</epage><pages>531-534</pages><issn>0028-0836</issn><eissn>1476-4687</eissn><coden>NATUAS</coden><abstract>Experimental autoimmune encephalomyelitis (EAE) is a prototype autoimmune disease mediated by type 1 helper T (T
H
1) cells and under the control of regulatory cells
1
,
2
,
3
. Here we report that a synthetic glycolipid ligand for CD1d-restricted natural killer T (NKT) cells expressing the semi-invariant T-cell receptor (Vα14
+
) is preventive against EAE. The ligand is an analogue of α-galactosylceramide (α-GC), a prototype NKT cell ligand, with a truncated sphingosine chain. α-GC causes NKT cells to produce both interferon (IFN)-γ and interleukin (IL)-4 (refs
4
,
5
). However, this new ligand can induce a predominant production of IL-4 by the NKT cells. A single injection of this glycolipid, but not of α-GC, consistently induced T
H
2 bias of autoimmune T cells by causing NKT cells to produce IL-4, leading to suppression of EAE. The lack of polymorphism of CD1d and cross-reactive response of mouse and human NKT cells to the same ligand
6
indicates that targeting NKT cells with this ligand may be an attractive means for intervening in human autoimmune diseases such as multiple sclerosis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>11586362</pmid><doi>10.1038/35097097</doi><tpages>4</tpages></addata></record> |
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| subjects | Amino Acid Sequence Animals Antigens, CD1 - immunology Antigens, CD1d Biological and medical sciences Encephalomyelitis, Autoimmune, Experimental - prevention & control Fundamental and applied biological sciences. Psychology Galactosylceramides - chemistry Glycolipids - chemistry Glycolipids - therapeutic use Humanities and Social Sciences Immunoglobulin G - immunology Interferon-gamma - biosynthesis Interferon-gamma - blood Interleukin-4 - biosynthesis Interleukin-4 - blood Killer Cells, Natural - immunology letter Ligands Lymphocyte Subsets - immunology Mice Molecular and cellular biology Molecular Sequence Data multidisciplinary Science Science (multidisciplinary) Th2 Cells - immunology |
| title | A synthetic glycolipid prevents autoimmune encephalomyelitis by inducing TH2 bias of natural killer T cells |
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