Control of Autoimmune Diabetes in NOD Mice by GAD Expression or Suppression in β Cells
Glutamic acid decarboxylase (GAD) is a pancreatic β cell autoantigen in humans and nonobese diabetic (NOD) mice. β Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the β cells in the othe...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 1999-05, Vol.284 (5417), p.1183-1187 |
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| creator | Yoon, Ji-Won Yoon, Chang-Soon Lim, Hye-Won Huang, Qi Quan Kang, Yup Pyun, Kwang Ho Hirasawa, Kensuke Sherwin, Robert S. Jun, Hee-Sook |
| description | Glutamic acid decarboxylase (GAD) is a pancreatic β cell autoantigen in humans and nonobese diabetic (NOD) mice. β Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the β cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of β cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, β cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes. |
| doi_str_mv | 10.1126/science.284.5417.1183 |
| format | Article |
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Complete suppression of β cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, β cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.284.5417.1183</identifier><identifier>PMID: 10325232</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Society for the Advancement of Science</publisher><subject>Adoptive Transfer ; Animals ; Autoantigens - genetics ; Autoantigens - immunology ; Autoantigens - physiology ; Autoimmune diseases ; Autoimmunity ; Biological and medical sciences ; Cell lines ; Diabetes ; Diabetes complications ; Diabetes Mellitus, Type 1 - enzymology ; Diabetes Mellitus, Type 1 - immunology ; Diabetes Mellitus, Type 1 - pathology ; Diabetes. Impaired glucose tolerance ; DNA, Antisense ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Gene Expression ; Glutamate decarboxylase ; Glutamate Decarboxylase - genetics ; Glutamate Decarboxylase - immunology ; Glutamate Decarboxylase - physiology ; Insulin ; Insulin - blood ; Insulin - metabolism ; Islets of Langerhans - enzymology ; Islets of Langerhans - immunology ; Islets of Langerhans - metabolism ; Islets of Langerhans - pathology ; Islets of Langerhans Transplantation ; Lymphocyte Activation ; Male ; Medical sciences ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Physiological aspects ; Prevention ; Splenocytes ; T lymphocytes ; T-Lymphocytes - immunology ; Transgenes ; Transgenic animals ; Type 1 diabetes ; Type 1 diabetes mellitus</subject><ispartof>Science (American Association for the Advancement of Science), 1999-05, Vol.284 (5417), p.1183-1187</ispartof><rights>Copyright 1999 American Association for the Advancement of Science</rights><rights>1999 INIST-CNRS</rights><rights>COPYRIGHT 1999 American Association for the Advancement of Science</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-d0f5ecde785a970804f44b33ab1263c5bf291e13dd3b758184c88d39a56d293a3</citedby><cites>FETCH-LOGICAL-c508t-d0f5ecde785a970804f44b33ab1263c5bf291e13dd3b758184c88d39a56d293a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/2899041$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/2899041$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,2871,2872,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1788209$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10325232$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoon, Ji-Won</creatorcontrib><creatorcontrib>Yoon, Chang-Soon</creatorcontrib><creatorcontrib>Lim, Hye-Won</creatorcontrib><creatorcontrib>Huang, Qi Quan</creatorcontrib><creatorcontrib>Kang, Yup</creatorcontrib><creatorcontrib>Pyun, Kwang Ho</creatorcontrib><creatorcontrib>Hirasawa, Kensuke</creatorcontrib><creatorcontrib>Sherwin, Robert S.</creatorcontrib><creatorcontrib>Jun, Hee-Sook</creatorcontrib><title>Control of Autoimmune Diabetes in NOD Mice by GAD Expression or Suppression in β Cells</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Glutamic acid decarboxylase (GAD) is a pancreatic β cell autoantigen in humans and nonobese diabetic (NOD) mice. β Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the β cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of β cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, β cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes.</description><subject>Adoptive Transfer</subject><subject>Animals</subject><subject>Autoantigens - genetics</subject><subject>Autoantigens - immunology</subject><subject>Autoantigens - physiology</subject><subject>Autoimmune diseases</subject><subject>Autoimmunity</subject><subject>Biological and medical sciences</subject><subject>Cell lines</subject><subject>Diabetes</subject><subject>Diabetes complications</subject><subject>Diabetes Mellitus, Type 1 - enzymology</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Diabetes Mellitus, Type 1 - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>DNA, Antisense</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Glutamate decarboxylase</subject><subject>Glutamate Decarboxylase - genetics</subject><subject>Glutamate Decarboxylase - immunology</subject><subject>Glutamate Decarboxylase - physiology</subject><subject>Insulin</subject><subject>Insulin - blood</subject><subject>Insulin - metabolism</subject><subject>Islets of Langerhans - enzymology</subject><subject>Islets of Langerhans - immunology</subject><subject>Islets of Langerhans - metabolism</subject><subject>Islets of Langerhans - pathology</subject><subject>Islets of Langerhans Transplantation</subject><subject>Lymphocyte Activation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>Mice, Transgenic</subject><subject>Physiological aspects</subject><subject>Prevention</subject><subject>Splenocytes</subject><subject>T lymphocytes</subject><subject>T-Lymphocytes - immunology</subject><subject>Transgenes</subject><subject>Transgenic animals</subject><subject>Type 1 diabetes</subject><subject>Type 1 diabetes mellitus</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0t1u0zAUB_AIgVg3eANAvkCIC1L82diXpR1lUlkvxsel5TgnlackLnYiba-1B-GZcJVqMGkSlS8sH_-OZVv_LHtN8JQQOvsYrYPOwpRKPhWcFKkq2ZNsQrASuaKYPc0mGLNZLnEhTrLTGK8xTnuKPc9OCGZUUEYn2c-F7_rgG-RrNB9679p26AAtnSmhh4hchy43S_TVWUDlLVrNl-j8ZhcgRuc75AO6Gnb3y4R_36EFNE18kT2rTRPh5WE-y75_Pv-2-JKvN6uLxXydW4Fln1e4FmArKKQwqsAS85rzkjFTpjcyK8qaKgKEVRUrCyGJ5FbKiikjZhVVzLCz7N147i74XwPEXrcu2nQD04Efop6p1MYU_i8kBeUc8yLBDyPcmga062rfB2O30EEwje-gdqk8F7yQrJjRxPNHeBoVtM4-5t8_8In0cNNvzRCjvri6PJpufhxNP62OpXK1fkDFSG3wMQao9S641oRbTbDep1AfUqhTCvU-hXqfwtT35vDXQ9lC9U_XGLsE3h6AidY0dTCddfGvK6SkWCX2amTXsffhfptKpTAn7A-VHetm</recordid><startdate>19990514</startdate><enddate>19990514</enddate><creator>Yoon, Ji-Won</creator><creator>Yoon, Chang-Soon</creator><creator>Lim, Hye-Won</creator><creator>Huang, Qi Quan</creator><creator>Kang, Yup</creator><creator>Pyun, Kwang Ho</creator><creator>Hirasawa, Kensuke</creator><creator>Sherwin, Robert S.</creator><creator>Jun, Hee-Sook</creator><general>American Society for the Advancement of Science</general><general>American Association for the Advancement of Science</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>8GL</scope><scope>IBG</scope><scope>IOV</scope><scope>ISN</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>19990514</creationdate><title>Control of Autoimmune Diabetes in NOD Mice by GAD Expression or Suppression in β Cells</title><author>Yoon, Ji-Won ; Yoon, Chang-Soon ; Lim, Hye-Won ; Huang, Qi Quan ; Kang, Yup ; Pyun, Kwang Ho ; Hirasawa, Kensuke ; Sherwin, Robert S. ; Jun, Hee-Sook</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-d0f5ecde785a970804f44b33ab1263c5bf291e13dd3b758184c88d39a56d293a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adoptive Transfer</topic><topic>Animals</topic><topic>Autoantigens - genetics</topic><topic>Autoantigens - immunology</topic><topic>Autoantigens - physiology</topic><topic>Autoimmune diseases</topic><topic>Autoimmunity</topic><topic>Biological and medical sciences</topic><topic>Cell lines</topic><topic>Diabetes</topic><topic>Diabetes complications</topic><topic>Diabetes Mellitus, Type 1 - enzymology</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Diabetes Mellitus, Type 1 - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>DNA, Antisense</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Glutamate decarboxylase</topic><topic>Glutamate Decarboxylase - genetics</topic><topic>Glutamate Decarboxylase - immunology</topic><topic>Glutamate Decarboxylase - physiology</topic><topic>Insulin</topic><topic>Insulin - blood</topic><topic>Insulin - metabolism</topic><topic>Islets of Langerhans - enzymology</topic><topic>Islets of Langerhans - immunology</topic><topic>Islets of Langerhans - metabolism</topic><topic>Islets of Langerhans - pathology</topic><topic>Islets of Langerhans Transplantation</topic><topic>Lymphocyte Activation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>Mice, Transgenic</topic><topic>Physiological aspects</topic><topic>Prevention</topic><topic>Splenocytes</topic><topic>T lymphocytes</topic><topic>T-Lymphocytes - immunology</topic><topic>Transgenes</topic><topic>Transgenic animals</topic><topic>Type 1 diabetes</topic><topic>Type 1 diabetes mellitus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoon, Ji-Won</creatorcontrib><creatorcontrib>Yoon, Chang-Soon</creatorcontrib><creatorcontrib>Lim, Hye-Won</creatorcontrib><creatorcontrib>Huang, Qi Quan</creatorcontrib><creatorcontrib>Kang, Yup</creatorcontrib><creatorcontrib>Pyun, Kwang Ho</creatorcontrib><creatorcontrib>Hirasawa, Kensuke</creatorcontrib><creatorcontrib>Sherwin, Robert S.</creatorcontrib><creatorcontrib>Jun, Hee-Sook</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>Gale In Context: High School</collection><collection>Gale In Context: Biography</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Canada</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Science (American Association for the Advancement of Science)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoon, Ji-Won</au><au>Yoon, Chang-Soon</au><au>Lim, Hye-Won</au><au>Huang, Qi Quan</au><au>Kang, Yup</au><au>Pyun, Kwang Ho</au><au>Hirasawa, Kensuke</au><au>Sherwin, Robert S.</au><au>Jun, Hee-Sook</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Control of Autoimmune Diabetes in NOD Mice by GAD Expression or Suppression in β Cells</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>1999-05-14</date><risdate>1999</risdate><volume>284</volume><issue>5417</issue><spage>1183</spage><epage>1187</epage><pages>1183-1187</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><coden>SCIEAS</coden><abstract>Glutamic acid decarboxylase (GAD) is a pancreatic β cell autoantigen in humans and nonobese diabetic (NOD) mice. β Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the β cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of β cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, β cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes.</abstract><cop>Washington, DC</cop><pub>American Society for the Advancement of Science</pub><pmid>10325232</pmid><doi>10.1126/science.284.5417.1183</doi><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0036-8075 |
| ispartof | Science (American Association for the Advancement of Science), 1999-05, Vol.284 (5417), p.1183-1187 |
| issn | 0036-8075 1095-9203 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_69758390 |
| source | American Association for the Advancement of Science; Jstor Complete Legacy; MEDLINE |
| subjects | Adoptive Transfer Animals Autoantigens - genetics Autoantigens - immunology Autoantigens - physiology Autoimmune diseases Autoimmunity Biological and medical sciences Cell lines Diabetes Diabetes complications Diabetes Mellitus, Type 1 - enzymology Diabetes Mellitus, Type 1 - immunology Diabetes Mellitus, Type 1 - pathology Diabetes. Impaired glucose tolerance DNA, Antisense Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Gene Expression Glutamate decarboxylase Glutamate Decarboxylase - genetics Glutamate Decarboxylase - immunology Glutamate Decarboxylase - physiology Insulin Insulin - blood Insulin - metabolism Islets of Langerhans - enzymology Islets of Langerhans - immunology Islets of Langerhans - metabolism Islets of Langerhans - pathology Islets of Langerhans Transplantation Lymphocyte Activation Male Medical sciences Mice Mice, Inbred NOD Mice, SCID Mice, Transgenic Physiological aspects Prevention Splenocytes T lymphocytes T-Lymphocytes - immunology Transgenes Transgenic animals Type 1 diabetes Type 1 diabetes mellitus |
| title | Control of Autoimmune Diabetes in NOD Mice by GAD Expression or Suppression in β Cells |
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