| pubmed-article:9933106 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9933106 | lifeskim:mentions | umls-concept:C0178539 | lld:lifeskim |
| pubmed-article:9933106 | lifeskim:mentions | umls-concept:C0011847 | lld:lifeskim |
| pubmed-article:9933106 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
| pubmed-article:9933106 | lifeskim:mentions | umls-concept:C0449258 | lld:lifeskim |
| pubmed-article:9933106 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
| pubmed-article:9933106 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:9933106 | pubmed:dateCreated | 1999-2-16 | lld:pubmed |
| pubmed-article:9933106 | pubmed:abstractText | Insulin-dependent diabetes mellitus (IDDM) is not a disease of unbridled destruction. The autoimmune attack on pancreatic beta cells has two distinct stages - insulitis and diabetes - and progression of the former to the latter appears to be highly regulated. Identifying the factors controlling this transition has been difficult because it is a complex process that occurs non-universally and asynchronously. We have overcome these difficulties by coupling a simplified TCR transgenic (tg) model of IDDM and the immunosuppressive drug cyclophosphamide (CY). Young BDC2.5 TCR tg mice show insulitis but not diabetes; CY treatment provoked diabetes in 100% of animals with rapid, highly reproducible kinetics. This allowed a detailed temporal analysis of changes in cellular organization and cytokine gene expression within the lesion. The monokines IL-18, IL-12 and TNF-alpha were pivotal, their induction occurring almost immediately and their coordinate action being required for the onset of aggression. Other cytokines with direct toxicity for beta cells, including IL-1 -beta, IL-6 and IFN-gamma, were subsequently induced; in contrast, there was no cellular or molecular evidence of cell contact-mediated mechanisms of beta cell death. | lld:pubmed |
| pubmed-article:9933106 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9933106 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9933106 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9933106 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9933106 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9933106 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:9933106 | pubmed:issn | 0014-2980 | lld:pubmed |
| pubmed-article:9933106 | pubmed:author | pubmed-author:BenoistCC | lld:pubmed |
| pubmed-article:9933106 | pubmed:author | pubmed-author:HindelangCC | lld:pubmed |
| pubmed-article:9933106 | pubmed:author | pubmed-author:MathisDD | lld:pubmed |
| pubmed-article:9933106 | pubmed:author | pubmed-author:André-Schmutz... | lld:pubmed |
| pubmed-article:9933106 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9933106 | pubmed:volume | 29 | lld:pubmed |
| pubmed-article:9933106 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9933106 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9933106 | pubmed:pagination | 245-55 | lld:pubmed |
| pubmed-article:9933106 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:9933106 | pubmed:meshHeading | pubmed-meshheading:9933106-... | lld:pubmed |
| pubmed-article:9933106 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:9933106 | pubmed:articleTitle | Cellular and molecular changes accompanying the progression from insulitis to diabetes. | lld:pubmed |
| pubmed-article:9933106 | pubmed:affiliation | Institut de Génétique et de Biologie Moléculaire et Cellulaire (CNRS/INSERM/ULP), Illkirch, France. | lld:pubmed |
| pubmed-article:9933106 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9933106 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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