Invasion of the killer B's in type 1 diabetes.

Document Type

Article

Publication Date

2007

Keywords

Antigen-Presenting-Cells, B-Lymphocyte-Subsets, B-Lymphocytes, CD4-Positive-T-Lymphocytes, Diabetes-Mellitus-Type-1, H-2-Antigens, Humans, Mice, Mice-Inbred-NOD

First Page

2183

Last Page

2193

JAX Location

see Reprint Collection (a pdf is available)

JAX Source

Front Biosci 2007; 12:2183-93.

Abstract

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.

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