Linked Life Data

12185667

Source:http://linkedlifedata.com/resource/pubmed/id/12185667

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-8-20
pubmed:abstractText
Type 1 diabetes mellitus is a T-cell-mediated autoimmune disease that results in the destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans. In spite of extensive genetic and immunological studies, mainly performed in the non-obese diabetic (NOD) spontaneous mouse model, the etiology of the autoimmune attack remains unknown. Several autoantigens have been identified and numerous studies have suggested a role for defective regulation of immune function. However, this account does not explain why the autoimmune process specifically affects the insulin-producing beta cells. Thus, abnormal immune regulation might explain the predisposition to autoimmunity in general, but additional factors should then determine the target of the autoimmune attack. Here, we review the evidence that abnormalities in islet cell differentiation and function exist that might trigger the immune system towards beta-cell autoimmunity in humans and NOD mice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1043-2760
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
209-14
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Islet abnormalities in the pathogenesis of autoimmune diabetes.
pubmed:affiliation
Dept Immunology, Erasmus MC, University Medical Center, PO Box 1738, 3000 DR Rotterdam, The Netherlands.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't