Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-11-25
pubmed:abstractText
Type I diabetes mellitus is an autoimmune disease mediated by a selective immune-mediated destruction of the insulin containing beta cells within the pancreatic islets of Langerhans. T cells reactive to beta cell-derived antigens are critical for the pathogenesis of type I diabetes, indeed treatments that target T cells are currently in clinical trials. CD8+ T cells may play a particularly crucial role in the onset of hyperglycaemia, as they can mediate beta cell destruction late in the pathogenesis of diabetes. However, the precise steps by which beta cell-reactive CD8+ T cells are activated are poorly understood. In this review we speculate on the possibility that B cells are essential for the activation and expansion of pathogenic CD8+ T cells that cause final beta cell destruction. We also discuss the involvement of different B cell subsets in the aetiology of diabetes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0896-8411
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
301-5
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
A new role for an old player: do B cells unleash the self-reactive CD8+ T cell storm necessary for the development of type 1 diabetes?
pubmed:affiliation
Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't