Streptozotocin Upregulates GAD67 Expression in MIN6N8a Mouse Beta Cells

IL‐23 leads to diabetes induction after subdiabetogenic treatment with multiple low doses of streptozotocin

“…Mice received MLD-STZ treatment as described previously [3,4]. Briefly, STZ was dissolved in citrate buffer, pH 4.5, and injected i.p.…”

“…While at high doses the diabetogenic potential of STZ is explained by its capacity to selectively promote insulin-producing b cell death by apoptosis or necrosis, at low doses, STZ generates H 2 O 2 [3] and induces expression of glutamic acid decarboxylase autoantigens [4]. Glutamic acid decarboxylase is a strong trigger of b cell-specific autoimmunity, both in humans and experimental models of diabetes [5][6][7].…”

T-cell vaccination leads to suppression of intrapancreatic Th17 cells through Stat3-mediated RORγt inhibition in autoimmune diabetes

“…While at high doses this agent has diabetogenic potential due to its capacity to selectively promote death of insulin-producing β cells by apoptosis or necrosis, at low doses, STZ generates hydrogen peroxide [20] and induces expression of the glutamic acid decarboxylase autoantigen [21]. Glutamic acid decarboxylase (GAD) is a strong trigger of β-cell-specific autoimmunity, both in humans and experimental models of diabetes [22][23][24].…”

Pam3CSK4 enhanced beta cell loss and diabetogenesis: The roles of IFN-gamma and IL-17

“…The lowest dose of 100 μg was employed by Patel et al [6] in their studies on TLR2 agonist on allergic airway inflammation in susceptible mice. Disease was monitored as described previously [11,12]. To determine whether Pam3CSK 4 promoted MLD-STZ diabetes, after subdiabetogenic doses, WT, IFN-γ −/− and IL-17 −/− mice were given 4 consecutive doses of STZ followed by 5 daily doses of Pam3CSK 4 .…”

“…Streptozotocin (STZ), a D-glucopyranose derivative of N-Methyl-N-nitrosourea at high dose selectively promotes insulin-producing β cell death by apoptosis or necrosis, but at low doses, generates H 2 O 2 [11] and induces expression of glutamic acid decarboxylase (GAD) autoantigens [12] in addition to very limited beta cell death. It has also been demonstrated that while five multiple low doses induce diabetes in susceptible strains of mice, the regime of four doses (subdiabetogenic) does not even induce diabetes though it causes limited β cell death [13].…”