A rat monoclonal antibody (mAb) that neutralizes mouse interleukin-12 (IL-12) was administered to female non-obese diabetic (NOD) mice of different ages to dismantle the role of endogenous IL-12 in murine autoimmune diabetogenesis. This mAb was effective in preventing clinical, but not histological signs of spontaneous diabetes when treatment was started early in life at the age of 4 weeks and consecutively continued for 10 weeks. Delaying commencement of anti-IL-12 mAb prophylaxis until the age of 18 weeks, when NOD mice suffer from advanced insulitis, was ineffective. Anti-IL-12 mAb did not influence the course of the accelerated model of diabetes induced by cyclophosphamide. These data prove that the pathogenetic role of endogenous IL-12 in NOD mouse diabetes is restricted to the very early diabetogenic events presumably occurring prior to insulitis development.
Endogenous interleukin-12 only plays a key pathogenetic role in non-obese diabetic mouse diabetes during the very early stages of the disease
NICOLETTI, FERDINANDO;Di Marco R;MAGRO, Gaetano Giuseppe;DI MAURO, Maurizio;
1999-01-01
Abstract
A rat monoclonal antibody (mAb) that neutralizes mouse interleukin-12 (IL-12) was administered to female non-obese diabetic (NOD) mice of different ages to dismantle the role of endogenous IL-12 in murine autoimmune diabetogenesis. This mAb was effective in preventing clinical, but not histological signs of spontaneous diabetes when treatment was started early in life at the age of 4 weeks and consecutively continued for 10 weeks. Delaying commencement of anti-IL-12 mAb prophylaxis until the age of 18 weeks, when NOD mice suffer from advanced insulitis, was ineffective. Anti-IL-12 mAb did not influence the course of the accelerated model of diabetes induced by cyclophosphamide. These data prove that the pathogenetic role of endogenous IL-12 in NOD mouse diabetes is restricted to the very early diabetogenic events presumably occurring prior to insulitis development.File | Dimensione | Formato | |
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