Linked Life Data

18568644

Source:http://linkedlifedata.com/resource/pubmed/id/18568644

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-6-23
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1607-842X
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
383-94
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Both central and peripheral tolerance mechanisms play roles in diabetes prevention in NOD-E transgenic mice.
pubmed:affiliation
Immunology Division, Department of Pathology, University of Cambridge, Cambridge, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't