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Establish the Regulatory Environment for the Control of Diabetogenic T Cells in the Nonobese Diabetic Mouse1
,¶,||
* Diabetes Research Center, Cincinnati Children’s Research Foundation, and
Division of Endocrinology,
Division of Rheumatology,
Division of Developmental Biology,
¶ Division of Ophthalmology, and
|| Division of Molecular Immunology, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45229
In type 1 diabetes mellitus (T1DM), T cell-mediated destruction of insulin-producing pancreatic 
cells leads to the acute onset of hyperglycemia. The nonobese diabetic mouse model of human T1DM reveals that T cells capable of inducing diabetes can escape normal central tolerance, and can cause T1DM if left unchecked. However, several regulatory T cell subsets can temper autoaggressive T cells, although it remains undetermined when and how, and by which subset, homeostatic control of diabetogenic T cells is normally achieved in vivo. Using a cotransfer model, we find that NKT cells efficiently dampen the action of diabetogenic CD4+ T cells, and do so in an indirect manner by modifying the host environment. Moreover, the NKT cell-containing population modifies the host via production of IFN-
that is necessary for driving the inhibition of diabetogenic T cells in vivo.
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