期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 12, 期 -, 页码 2183-2193出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/2221
关键词
immune system; immunity; autoimmunity; diabetes; B cells; T cells; tolerance; mice; review
资金
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK051090, R29DK046266, R01DK046266] Funding Source: NIH RePORTER
- NIDDK NIH HHS [DK51090, DK46266] Funding Source: Medline
Type 1 Diabetes ( T1D) is an autoimmune disease requiring contributions from effectors in both CD4(+) and CD8(+) T cell compartments in order to destroy insulin producing pancreatic beta cells. Autoantibodies specific for islet cell proteins are also often generated during the prodromal stages of T1D development. While providing excellent prognostic markers of future disease risk, it has generally been believed that the induction of autoantibody secretion by B cells was a secondary consequence of the ongoing autoreactive T cell response. However, studies in the NOD mouse model of disease have demonstrated that B cells play a key function during T1D development by serving as a subpopulation of antigen presenting cell ( APC) which can most efficiently support the expansion of diabetogenic CD4(+) T cells. Furthermore, studies utilizing this model have indicated that autoantibodies may play an important role in initiating an early phase of pancreatic beta cell destruction ultimately leading to overt T1D. This review will focus on the under appreciated role B cells play in T1D development not only in NOD mice, but also potentially in humans.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据