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?
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.
|Authors||Marino, E.; Grey, S. T.|
|Publisher Name||JOURNAL OF AUTOIMMUNITY|
|URL link to publisher's version||cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18809297|
|OpenAccess link to author's accepted manuscript version||https://publications.gimr.garvan.org.au/open-access/10072|