Tissue-targeted therapy of autoimmune diabetes using dendritic cells transduced to express IL-4 in NOD mice
Abstract A deficit in IL-4 production has been previously reported in both diabetic human patients and non-obese diabetic (NOD) mice. In addition, re-introducing IL-4 into NOD mice systemically, or as a transgene, led to a beneficial outcome in most studies. Here, we show that prediabetic, 12-week o...
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| Veröffentlicht in: | Clinical immunology (Orlando, Fla.) Fla.), 2008-05, Vol.127 (2), p.176-187 |
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| creator | Creusot, Rémi J Yaghoubi, Shahriar S Kodama, Keiichi Dang, Demi N Dang, Vu H Breckpot, Karine Thielemans, Kris Gambhir, Sanjiv S Fathman, C. Garrison |
| description | Abstract A deficit in IL-4 production has been previously reported in both diabetic human patients and non-obese diabetic (NOD) mice. In addition, re-introducing IL-4 into NOD mice systemically, or as a transgene, led to a beneficial outcome in most studies. Here, we show that prediabetic, 12-week old female NOD mice have a deficit in IL-4 expression in the pancreatic lymph nodes (PLN) compared to age-matched diabetes-resistant NOD.B10 mice. By bioluminescence imaging, we demonstrated that the PLN was preferentially targeted by bone marrow-derived dendritic cells (DCs) following intravenous (IV) administration. Following IV injection of DCs transduced to express IL-4 (DC/IL-4) into 12-week old NOD mice, it was possible to significantly delay or prevent the onset of hyperglycemia. We then focused on the PLN to monitor, by microarray analysis, changes in gene expression induced by DC/IL-4 and observed a rapid normalization of the expression of many genes, that were otherwise under-expressed compared to NOD.B10 PLN. The protective effect of DC/IL-4 required both MHC and IL-4 expression by the DCs. Thus, adoptive cellular therapy, using DCs modified to express IL-4, offers an effective, tissue-targeted cellular therapy to prevent diabetes in NOD mice at an advanced stage of pre-diabetes, and may offer a safe approach to consider for treatment of high risk human pre-diabetic patients. |
| doi_str_mv | 10.1016/j.clim.2007.12.009 |
| format | Article |
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Garrison</creator><creatorcontrib>Creusot, Rémi J ; Yaghoubi, Shahriar S ; Kodama, Keiichi ; Dang, Demi N ; Dang, Vu H ; Breckpot, Karine ; Thielemans, Kris ; Gambhir, Sanjiv S ; Fathman, C. Garrison</creatorcontrib><description>Abstract A deficit in IL-4 production has been previously reported in both diabetic human patients and non-obese diabetic (NOD) mice. In addition, re-introducing IL-4 into NOD mice systemically, or as a transgene, led to a beneficial outcome in most studies. Here, we show that prediabetic, 12-week old female NOD mice have a deficit in IL-4 expression in the pancreatic lymph nodes (PLN) compared to age-matched diabetes-resistant NOD.B10 mice. By bioluminescence imaging, we demonstrated that the PLN was preferentially targeted by bone marrow-derived dendritic cells (DCs) following intravenous (IV) administration. Following IV injection of DCs transduced to express IL-4 (DC/IL-4) into 12-week old NOD mice, it was possible to significantly delay or prevent the onset of hyperglycemia. We then focused on the PLN to monitor, by microarray analysis, changes in gene expression induced by DC/IL-4 and observed a rapid normalization of the expression of many genes, that were otherwise under-expressed compared to NOD.B10 PLN. The protective effect of DC/IL-4 required both MHC and IL-4 expression by the DCs. Thus, adoptive cellular therapy, using DCs modified to express IL-4, offers an effective, tissue-targeted cellular therapy to prevent diabetes in NOD mice at an advanced stage of pre-diabetes, and may offer a safe approach to consider for treatment of high risk human pre-diabetic patients.</description><identifier>ISSN: 1521-6616</identifier><identifier>EISSN: 1521-7035</identifier><identifier>DOI: 10.1016/j.clim.2007.12.009</identifier><identifier>PMID: 18337172</identifier><identifier>CODEN: CLIIFY</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Allergy and Immunology ; Animals ; Biological and medical sciences ; Bioluminescence ; Blood Glucose - analysis ; Cellular gene therapy ; Dendritic cell ; Dendritic Cells - immunology ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - immunology ; Diabetes Mellitus, Type 1 - prevention & control ; Diabetes Mellitus, Type 1 - therapy ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Gene Expression ; Genetic Therapy ; Histocompatibility Antigens - immunology ; Immunotherapy, Adoptive - methods ; Interleukin-4 ; Interleukin-4 - biosynthesis ; Interleukin-4 - deficiency ; Interleukin-4 - genetics ; Interleukin-4 - immunology ; Lymph Nodes - immunology ; Medical sciences ; Mice ; Mice, Inbred NOD ; NOD mouse ; Oligonucleotide Array Sequence Analysis ; Pancreas - immunology ; Pancreatic lymph node ; Prediabetic State - genetics ; Prediabetic State - immunology ; Prediabetic State - therapy ; Reverse Transcriptase Polymerase Chain Reaction ; RNA - chemistry ; RNA - genetics ; Transduction, Genetic ; Type 1 diabetes</subject><ispartof>Clinical immunology (Orlando, Fla.), 2008-05, Vol.127 (2), p.176-187</ispartof><rights>Elsevier Inc.</rights><rights>2008 Elsevier Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c635t-5bb4745d716b2e05217e061752d3d8022281e7c6456aa2b0eb0e39950349f3443</citedby><cites>FETCH-LOGICAL-c635t-5bb4745d716b2e05217e061752d3d8022281e7c6456aa2b0eb0e39950349f3443</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.clim.2007.12.009$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20291888$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18337172$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Creusot, Rémi J</creatorcontrib><creatorcontrib>Yaghoubi, Shahriar S</creatorcontrib><creatorcontrib>Kodama, Keiichi</creatorcontrib><creatorcontrib>Dang, Demi N</creatorcontrib><creatorcontrib>Dang, Vu H</creatorcontrib><creatorcontrib>Breckpot, Karine</creatorcontrib><creatorcontrib>Thielemans, Kris</creatorcontrib><creatorcontrib>Gambhir, Sanjiv S</creatorcontrib><creatorcontrib>Fathman, C. Garrison</creatorcontrib><title>Tissue-targeted therapy of autoimmune diabetes using dendritic cells transduced to express IL-4 in NOD mice</title><title>Clinical immunology (Orlando, Fla.)</title><addtitle>Clin Immunol</addtitle><description>Abstract A deficit in IL-4 production has been previously reported in both diabetic human patients and non-obese diabetic (NOD) mice. In addition, re-introducing IL-4 into NOD mice systemically, or as a transgene, led to a beneficial outcome in most studies. Here, we show that prediabetic, 12-week old female NOD mice have a deficit in IL-4 expression in the pancreatic lymph nodes (PLN) compared to age-matched diabetes-resistant NOD.B10 mice. By bioluminescence imaging, we demonstrated that the PLN was preferentially targeted by bone marrow-derived dendritic cells (DCs) following intravenous (IV) administration. Following IV injection of DCs transduced to express IL-4 (DC/IL-4) into 12-week old NOD mice, it was possible to significantly delay or prevent the onset of hyperglycemia. We then focused on the PLN to monitor, by microarray analysis, changes in gene expression induced by DC/IL-4 and observed a rapid normalization of the expression of many genes, that were otherwise under-expressed compared to NOD.B10 PLN. The protective effect of DC/IL-4 required both MHC and IL-4 expression by the DCs. Thus, adoptive cellular therapy, using DCs modified to express IL-4, offers an effective, tissue-targeted cellular therapy to prevent diabetes in NOD mice at an advanced stage of pre-diabetes, and may offer a safe approach to consider for treatment of high risk human pre-diabetic patients.</description><subject>Allergy and Immunology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bioluminescence</subject><subject>Blood Glucose - analysis</subject><subject>Cellular gene therapy</subject><subject>Dendritic cell</subject><subject>Dendritic Cells - immunology</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Diabetes Mellitus, Type 1 - prevention & control</subject><subject>Diabetes Mellitus, Type 1 - therapy</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Gene Expression</subject><subject>Genetic Therapy</subject><subject>Histocompatibility Antigens - immunology</subject><subject>Immunotherapy, Adoptive - methods</subject><subject>Interleukin-4</subject><subject>Interleukin-4 - biosynthesis</subject><subject>Interleukin-4 - deficiency</subject><subject>Interleukin-4 - genetics</subject><subject>Interleukin-4 - immunology</subject><subject>Lymph Nodes - immunology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>NOD mouse</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Pancreas - immunology</subject><subject>Pancreatic lymph node</subject><subject>Prediabetic State - genetics</subject><subject>Prediabetic State - immunology</subject><subject>Prediabetic State - therapy</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA - chemistry</subject><subject>RNA - genetics</subject><subject>Transduction, Genetic</subject><subject>Type 1 diabetes</subject><issn>1521-6616</issn><issn>1521-7035</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkk1r3DAQhk1padK0f6CHokt7szuSbMmGEgjpV2BpDk3PQpZnN9rY8lZjh-6_r8wu6cehFAQSzPPOh97JspccCg5cvd0WrvdDIQB0wUUB0DzKTnkleK5BVo-Pb6W4OsmeEW0BoBJCPc1OeC2l5lqcZnc3nmjGfLJxgxN2bLrFaHd7Nq6ZnafRD8MckHXetilMbCYfNqzD0EU_eccc9j2xKdpA3ewW_cjwxy4iEbta5SXzgX25fs8G7_B59mRte8IXx_ss-_bxw83l53x1_enq8mKVOyWrKa_attRl1WmuWoGpZa4RFNeV6GRXgxCi5qidKitlrWgB05FNU4Esm7UsS3mWnR_y7uZ2wM5hSP31Zhf9YOPejNabPyPB35rNeG9EWUnQKiV4c0wQx-8z0mQGT8ukNuA4k9FQNqr8D1BAGgJEk0BxAF0ciSKuH7rhYBYzzdYsZprFTMOFSWYm0avf5_glObqXgNdHwJKz_Tq54Dw9cCJV5nVdJ-7dgcP06_ceoyHnMSS7fEQ3mW70_-7j_C95QoJPFe9wj7Qd5xiSn4YbSgLzdVm7ZeugThsHopY_AZnu0kw</recordid><startdate>20080501</startdate><enddate>20080501</enddate><creator>Creusot, Rémi J</creator><creator>Yaghoubi, Shahriar S</creator><creator>Kodama, Keiichi</creator><creator>Dang, Demi N</creator><creator>Dang, Vu H</creator><creator>Breckpot, Karine</creator><creator>Thielemans, Kris</creator><creator>Gambhir, Sanjiv S</creator><creator>Fathman, C. 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Garrison</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c635t-5bb4745d716b2e05217e061752d3d8022281e7c6456aa2b0eb0e39950349f3443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Allergy and Immunology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bioluminescence</topic><topic>Blood Glucose - analysis</topic><topic>Cellular gene therapy</topic><topic>Dendritic cell</topic><topic>Dendritic Cells - immunology</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Diabetes Mellitus, Type 1 - prevention & control</topic><topic>Diabetes Mellitus, Type 1 - therapy</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Gene Expression</topic><topic>Genetic Therapy</topic><topic>Histocompatibility Antigens - immunology</topic><topic>Immunotherapy, Adoptive - methods</topic><topic>Interleukin-4</topic><topic>Interleukin-4 - biosynthesis</topic><topic>Interleukin-4 - deficiency</topic><topic>Interleukin-4 - genetics</topic><topic>Interleukin-4 - immunology</topic><topic>Lymph Nodes - immunology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>NOD mouse</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Pancreas - immunology</topic><topic>Pancreatic lymph node</topic><topic>Prediabetic State - genetics</topic><topic>Prediabetic State - immunology</topic><topic>Prediabetic State - therapy</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA - chemistry</topic><topic>RNA - genetics</topic><topic>Transduction, Genetic</topic><topic>Type 1 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Creusot, Rémi J</creatorcontrib><creatorcontrib>Yaghoubi, Shahriar S</creatorcontrib><creatorcontrib>Kodama, Keiichi</creatorcontrib><creatorcontrib>Dang, Demi N</creatorcontrib><creatorcontrib>Dang, Vu H</creatorcontrib><creatorcontrib>Breckpot, Karine</creatorcontrib><creatorcontrib>Thielemans, Kris</creatorcontrib><creatorcontrib>Gambhir, Sanjiv S</creatorcontrib><creatorcontrib>Fathman, C. 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Garrison</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tissue-targeted therapy of autoimmune diabetes using dendritic cells transduced to express IL-4 in NOD mice</atitle><jtitle>Clinical immunology (Orlando, Fla.)</jtitle><addtitle>Clin Immunol</addtitle><date>2008-05-01</date><risdate>2008</risdate><volume>127</volume><issue>2</issue><spage>176</spage><epage>187</epage><pages>176-187</pages><issn>1521-6616</issn><eissn>1521-7035</eissn><coden>CLIIFY</coden><abstract>Abstract A deficit in IL-4 production has been previously reported in both diabetic human patients and non-obese diabetic (NOD) mice. In addition, re-introducing IL-4 into NOD mice systemically, or as a transgene, led to a beneficial outcome in most studies. Here, we show that prediabetic, 12-week old female NOD mice have a deficit in IL-4 expression in the pancreatic lymph nodes (PLN) compared to age-matched diabetes-resistant NOD.B10 mice. By bioluminescence imaging, we demonstrated that the PLN was preferentially targeted by bone marrow-derived dendritic cells (DCs) following intravenous (IV) administration. Following IV injection of DCs transduced to express IL-4 (DC/IL-4) into 12-week old NOD mice, it was possible to significantly delay or prevent the onset of hyperglycemia. We then focused on the PLN to monitor, by microarray analysis, changes in gene expression induced by DC/IL-4 and observed a rapid normalization of the expression of many genes, that were otherwise under-expressed compared to NOD.B10 PLN. The protective effect of DC/IL-4 required both MHC and IL-4 expression by the DCs. Thus, adoptive cellular therapy, using DCs modified to express IL-4, offers an effective, tissue-targeted cellular therapy to prevent diabetes in NOD mice at an advanced stage of pre-diabetes, and may offer a safe approach to consider for treatment of high risk human pre-diabetic patients.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>18337172</pmid><doi>10.1016/j.clim.2007.12.009</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Allergy and Immunology Animals Biological and medical sciences Bioluminescence Blood Glucose - analysis Cellular gene therapy Dendritic cell Dendritic Cells - immunology Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Diabetes Mellitus, Type 1 - prevention & control Diabetes Mellitus, Type 1 - therapy Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Fundamental and applied biological sciences. Psychology Fundamental immunology Gene Expression Genetic Therapy Histocompatibility Antigens - immunology Immunotherapy, Adoptive - methods Interleukin-4 Interleukin-4 - biosynthesis Interleukin-4 - deficiency Interleukin-4 - genetics Interleukin-4 - immunology Lymph Nodes - immunology Medical sciences Mice Mice, Inbred NOD NOD mouse Oligonucleotide Array Sequence Analysis Pancreas - immunology Pancreatic lymph node Prediabetic State - genetics Prediabetic State - immunology Prediabetic State - therapy Reverse Transcriptase Polymerase Chain Reaction RNA - chemistry RNA - genetics Transduction, Genetic Type 1 diabetes |
| title | Tissue-targeted therapy of autoimmune diabetes using dendritic cells transduced to express IL-4 in NOD mice |
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