| pubmed-article:20174617 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20174617 | lifeskim:mentions | umls-concept:C0085243 | lld:lifeskim |
| pubmed-article:20174617 | lifeskim:mentions | umls-concept:C0052441 | lld:lifeskim |
| pubmed-article:20174617 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:20174617 | lifeskim:mentions | umls-concept:C0229783 | lld:lifeskim |
| pubmed-article:20174617 | lifeskim:mentions | umls-concept:C0039635 | lld:lifeskim |
| pubmed-article:20174617 | lifeskim:mentions | umls-concept:C0011847 | lld:lifeskim |
| pubmed-article:20174617 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:20174617 | lifeskim:mentions | umls-concept:C1416467 | lld:lifeskim |
| pubmed-article:20174617 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:20174617 | lifeskim:mentions | umls-concept:C1292733 | lld:lifeskim |
| pubmed-article:20174617 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:20174617 | pubmed:dateCreated | 2010-7-23 | lld:pubmed |
| pubmed-article:20174617 | pubmed:abstractText | The ligand-activated transcription factor, aryl hydrocarbon receptor (AHR), is a novel inducer of adaptive Tregs. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the most potent AHR ligand, induces adaptive CD4+CD25+ Tregs during an acute graft-versus-host (GvH) response and prevents the generation of allospecific cytotoxic T lymphocytes. TCDD also suppresses the induction of experimental autoimmune encephalitis in association with an expanded population of Foxp3+ Tregs. In this study, we show that chronic treatment of NOD mice with TCDD potently suppresses the development of autoimmune Type 1 diabetes in parallel with greatly reduced pancreatic islet insulitis and an expanded population of CD4+CD25+Foxp3+ cells in the pancreatic lymph nodes. When treatment with TCDD was terminated after 15 weeks (23 weeks of age), mice developed diabetes over the next 8 weeks in association with lower numbers of Tregs and decreased activation of AHR. Analysis of the expression levels of several genes associated with inflammation, T-cell activation and/or Treg function in pancreatic lymph node cells failed to reveal any differences associated with TCDD treatment. Taken together, the data suggest that AHR activation by TCDD-like ligands may represent a novel avenue for treatment of immune-mediated diseases. | lld:pubmed |
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| pubmed-article:20174617 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:20174617 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20174617 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:20174617 | pubmed:issn | 1750-7448 | lld:pubmed |
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| pubmed-article:20174617 | pubmed:author | pubmed-author:FarrerDavidD | lld:pubmed |
| pubmed-article:20174617 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20174617 | pubmed:volume | 1 | lld:pubmed |
| pubmed-article:20174617 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20174617 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20174617 | pubmed:pagination | 539-47 | lld:pubmed |
| pubmed-article:20174617 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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| pubmed-article:20174617 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:20174617 | pubmed:articleTitle | Activation of aryl hydrocarbon receptor by TCDD prevents diabetes in NOD mice and increases Foxp3+ T cells in pancreatic lymph nodes. | lld:pubmed |
| pubmed-article:20174617 | pubmed:affiliation | Oregon State University, Department of Microbiology, Corvallis, OR 97331, USA. | lld:pubmed |
| pubmed-article:20174617 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20174617 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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