Abstract
Development of Type I diabetes results from an autoimmune attack of islet cell antigen specific T helper I (Th I) cells and scavenger macrophages directed towards β-cells f islets of Langerhans. Such an aggressive Th I response can be downregulated by other subsets of so-called regulatory or suppressor T-cells, amongst which are the Th 2 cells. In the BB rat model of Type I diabetes such regulatory T-cells reside in the RT6+T-cell pool, since transfer of such cells from diabetes-resistant rats (BB-DP rats) prevents the development of the disease. Dentric cells (CD), the antigen-presenting cells (APC) par excellence play a pivotal role in the initial triggering of islet-specific T-cells in the Type I diabetic process: [...]
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