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- W2088876216 abstract "The cellular and molecular requirements for β -cell damages in an immune-mediated toxininduced insulin-dependent diabetes mellitus have been studied in the model of multiple low-dose streptozotocin-induced diabetes in rats and mice. It was found that strain-related susceptibility to diabetes induction correlated with a higher level of IL-2, IFN- γ , and TNF- α production, whereas such differences were not observed when IL-1 and NO production by macrophages were analyzed; elimination of immunoregulatory RT6 + T cells that increases IFN- γ production, enhances susceptibility to MLD-STZ-induced diabetes; mercury-induced Th-2 cells downregulated the disease; IFN- γ -mediated macrophage activation to produce proinflammatory cytokines rather than NO is an important event in early diabetogenic effects of invading macrophages; inhibition of IL-1 activity downregulates diabetes induction; and generation of NO in β cells appears to be important for diabetogenic effects. Taken together, data indicate that MLD-STZ diabetes is induced by Th-1 lymphocytes that secrete soluble effector molecules that activate macrophages and promote destruction of β cells possibly by both nitric oxide and nonnitric oxide-mediated mechanisms." @default.
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- W2088876216 date "1998-01-01" @default.
- W2088876216 modified "2023-10-12" @default.
- W2088876216 title "Effector Mechanisms in Low-Dose Streptozotocin-induced Diabetes" @default.
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- W2088876216 doi "https://doi.org/10.1155/1998/92198" @default.
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