Linked Life Data

16580840

Source:http://linkedlifedata.com/resource/pubmed/id/16580840

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-5-8
pubmed:abstractText
It has long been established that type 1 diabetes (T1D) is a T cell-mediated autoimmune disease, with CD4+ and CD8+ T cells being largely responsible for the destruction of beta cells within the pancreatic islets of Langerhans. Although autoantibodies specific for islet cell proteins are regularly detected in individuals with T1D and can be utilized as effective markers for predicting the onset of disease, they are not believed to be directly pathogenic to beta cells. Thus, activation of autoantibody-secreting B cells has long been regarded as a secondary consequence of the ongoing self-reactive T cell response. However, recently, studies in the nonobese diabetic mouse model of disease have demonstrated that B cells are an important component in the development of T1D by virtue of their ability to act as the preferential antigen presenting cell population required for efficient expansion of diabetogenic CD4+ T cells. Furthermore, autoantibodies might also be responsible for mediating early beta cell pathogenesis in this model.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1043-2760
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
128-35
pubmed:dateRevised
2009-9-28
pubmed:meshHeading
pubmed:articleTitle
B cells in the spotlight: innocent bystanders or major players in the pathogenesis of type 1 diabetes.
pubmed:affiliation
Immunology and Inflammation Program, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010, Australia. p.silveira@garvan.org.au
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't