Anti-islet autoantibodies trigger autoimmune diabetes in the presence of an increased frequency of islet-reactive CD4 T cells.

ABSTRACT:

Objective

To define cellular mechanisms by which B cells promote type 1 diabetes.

Research design and methods

The study measured islet-specific CD4 T cell regulation in T-cell receptor transgenic mice with elevated frequencies of CD4 T cells recognizing hen egg lysozyme (HEL) autoantigen expressed in islet β-cells and thymic epithelium under control of the insulin-gene promoter. The effects of a mutation in Roquin that dysregulates T follicular helper (Tfh) cells to promote B-cell activation and anti-islet autoantibodies were studied, as were the effects of HEL antigen-presenting B cells and passively transferred or maternally transmitted anti-islet HEL antibodies.

Results

Mouse anti-islet IgG antibodies-either formed as a consequence of excessive Tfh activity, matern

SUBMITTER: Silva DG 

PROVIDER: S-EPMC3142068 | biostudies-literature | 2011 Aug

REPOSITORIES: biostudies-literature