pubmed-article:18568644 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18568644 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:18568644 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
pubmed-article:18568644 | lifeskim:mentions | umls-concept:C0032214 | lld:lifeskim |
pubmed-article:18568644 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
pubmed-article:18568644 | lifeskim:mentions | umls-concept:C0205100 | lld:lifeskim |
pubmed-article:18568644 | lifeskim:mentions | umls-concept:C1659987 | lld:lifeskim |
pubmed-article:18568644 | lifeskim:mentions | umls-concept:C0205099 | lld:lifeskim |
pubmed-article:18568644 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:18568644 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:18568644 | pubmed:dateCreated | 2008-6-23 | lld:pubmed |
pubmed-article:18568644 | pubmed:abstractText | The non-obese diabetic (NOD) mouse spontaneously develops diabetes and is a widely used model of Type 1 Diabetes in humans. The major histocompatibility complex class II plays an important role in governing disease susceptibility in NOD mice. NOD mice express a rare I-A allele, I-A(g7), and do not express I-E molecules. Interestingly, transgenic NOD mice which express I-E (NOD-E) fail to develop diabetes although, the protective mechanism(s) are incompletely understood. Initially, we explored whether diabetes prevention was due to deletion of autoreactive T cells. Through adoptive transfer with depletion of CD25+ T cells, we demonstrated that autoreactive T cells were present in the periphery of NOD-E mice. Although, BDC2.5NOD T cells proliferated less in the pancreatic lymph nodes of NOD-E mice, we found that they transferred disease with a similar kinetic in NOD.scid and NOD-E.scid recipients suggesting that there was little difference in peripheral antigen presentation in NOD-E mice. We also found that there were no proportional or functional differences between NOD and NOD-E T regs. Our studies indicate that autoreactive T cells are present within the periphery of NOD-E mice but that these cells are present in low numbers suggesting that peripheral tolerogenic mechanisms are able to prevent them from inducing diabetes. | lld:pubmed |
pubmed-article:18568644 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18568644 | pubmed:language | eng | lld:pubmed |
pubmed-article:18568644 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18568644 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18568644 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18568644 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18568644 | pubmed:month | Aug | lld:pubmed |
pubmed-article:18568644 | pubmed:issn | 1607-842X | lld:pubmed |
pubmed-article:18568644 | pubmed:author | pubmed-author:CookeAnneA | lld:pubmed |
pubmed-article:18568644 | pubmed:author | pubmed-author:PhillipsJenny... | lld:pubmed |
pubmed-article:18568644 | pubmed:author | pubmed-author:MellanbyRicha... | lld:pubmed |
pubmed-article:18568644 | pubmed:author | pubmed-author:ParishNicole... | lld:pubmed |
pubmed-article:18568644 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18568644 | pubmed:volume | 41 | lld:pubmed |
pubmed-article:18568644 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18568644 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18568644 | pubmed:pagination | 383-94 | lld:pubmed |
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pubmed-article:18568644 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18568644 | pubmed:articleTitle | Both central and peripheral tolerance mechanisms play roles in diabetes prevention in NOD-E transgenic mice. | lld:pubmed |
pubmed-article:18568644 | pubmed:affiliation | Immunology Division, Department of Pathology, University of Cambridge, Cambridge, UK. | lld:pubmed |
pubmed-article:18568644 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18568644 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |