Terry L. Delovitch

TL;DR: The key to the onset of immune dysregulation and aberrant increase in the number of autoreactive T cells in the periphery may be that the activation threshold required for TCR-stimulation is markedly increased in T cells from NOD mice and humans with IDDM.

TL;DR: It is shown that α-GalCer treatment, even when initiated after the onset of insulitis, protects female N OD mice from T1D and prolongs the survival of pancreatic islets transplanted into newly diabetic NOD mice, raising the possibility thatα-galactosylceramide treatment might be used therapeutically to prevent the onset and recurrence of human T1d.

TL;DR: The ability of rIL-4 to reverse completely the NOD thymic and peripheral T cell proliferative defect in vitro and protect against diabetes in vivo provides further support for a causal relationship between this T cell Proliferative unresponsiveness and susceptibility to diabetes in NOD mice.

TL;DR: The potential importance of interactions between CD1D-restricted natural killer T (iNKT) cells and dendritic cells (DCs) has been discussed in this paper, which indicates that iNKT cells regulate DC activity to shape both pro-inflammatory and tolerogenic immune responses.

TL;DR: IL-4 treatment favors the expansion of regulatory CD4+ Th2 cells in vivo and prevents the onset of insulitis and IDDM mediated by autoreactive Th1 cells.