Cyclophosphamide-induced diabetes in NOD/WEHI mice. Evidence for suppression in spontaneous autoimmune diabetes mellitus.

摘要: Nonobese diabetic (NOD) mice spontaneously develop a lymphocytic infiltration of pancreatic islets (insulitis) that may progress to overt diabetes. Virtually all NOD/WEHI insulitis, but very few However, cyclophosphamide (CY) can promote the onset diabetes in NOD mice, including strain. The means by which CY produces was investigated it hypothesized active suppression mechanisms prevented progression from insulitis A study time course after given showed initially reduced rapidly increased over 16 days, and T-lymphocytes were predominant lesion. This suggested compression normal disease seen mice. did not produce any 11 non-NOD strains studied. Fetal isografts several days before subjected β-cell destruction. These findings directly (β-cell toxic altered β-cells essential for further demonstrated with subdiabetogenic doses streptozocin, significantly damaged increase severity or induce as CY. Most important, transfer mononuclear cells nondiabetic diabetes, indicated likely effect via immunomodulation, possibly allowing poised effector act on (β-cells. appear have suppressor acting halt early lesion so preventing occurring most We propose removes these suppressors thereby induces rapid compressing immune destruction process into 2-wk period. model affords opportunity ways practicable usual events.