| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Outline of Final Research Achievements |
Type 1 diabetes (T1D) is currently an incurable disease as other most autoimmune diseases. The pathology of T1D progresses from a silent prodromal phase to a clinical phase in which insulin-producing pancreatic β cells is destructed by autoreactive T cells. In this study, we demonstrated that an agonistic monoclonal antibody (mAb) to Toll-like receptor 4 (TLR4) prevents from the onset of T1D by prophylactic treatment and also reverses the new-onset of T1D by therapeutic treatment in nonobese diabetic mice. An agonistic TLR4 mAb induces the tolerance in innate immunity via dendritic cells and myeloid-derived suppressor cells, which results in the suppression of autoimmune T cells. In addition, regulatory T cells are also induced by agonistic TLR4 mAb in both periphery and pancreatic islets. These results propose that a tolerance induction through innate immunity by TLR4 mAb may be a novel immunological approach to cure the autoimmune pathology in T1D.
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