Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-11-27
pubmed:abstractText
The non-obese diabetic (NOD) mouse is an animal model of insulin-dependent diabetes mellitus (IDDM) that shows many of the characteristics of human IDDM. In the NOD model, there exists a discrepancy between the onset of insulitis and diabetes suggesting the potential existence of some form of immune regulation that delays beta cell destruction. Our transfer system using NOD-scid/scid (NOD-scid) mice as recipients of donor NOD cells suggested that immune regulatory cells exist in the periphery of NOD mice, not in the islets. These regulatory cells are considered to be memory CD4+ cells which show a Th2 (or Th zero) type cytokine profile following activation in vitro. The function of the memory CD4+ cells seems to change from protective to pathogenic as the disease progresses. Moreover, cytokine profiles of this CD4+ CD45RBlow (memory) population shifted from a Th2 (or Th zero) to a Th1 type response coincident with the onset of hyperglycaemia. These data suggest that the progression of NOD disease from insulitis to frank hyperglycaemia is under the control of CD4+ CD45RBlow immune 'regulatory' cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0896-8411
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
263-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Immune regulation in type 1 diabetes.
pubmed:affiliation
Department of Medicine, Stanford University School of Medicine, CA 94305, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't