| Project/Area Number |
22790865
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Metabolomics
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| Research Institution | 独立行政法人国立病院機構長崎医療センター臨床研究センター (2011)
Nagasaki University (2010) |
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Principal Investigator |
KURIYA Genpei 独立行政法人国立病院機構長崎医療センター臨床研究センター, 内科, 医師 (50457579)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | 1型糖尿病 / IL-17 / NODマウス |
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| Research Abstract |
T helper type 17(Th17) cells have been shown to play important roles in mouse models of several autoimmune diseases that had previously been thought Th1-dominant. In the NOD mouse, however, the relevance of IL-17/Th17 is still controversial, because of their inherent plasticity. Th17 cells derived from BDC2.5 NOD mice transfer diabetes through conversion to Th1 cells in vivo. We here studied the impact of IL-17 single-deficiency or IL-17/IFN-γreceptor double-deficiency on the development of insulitis/diabetes in NOD mice. IL-17 single-deficiency significantly delayed the onset of diabetes and attenuated the severity of insulitis, but the cumulative incidence of diabetes until 50 weeks of age in IL-17 deficient mice was similar to that in wild-type(wt) mice. Adoptive transfer study with CD4+CD25-T cells from young non-diabetic IL-17 single-deficient NOD mice, but not that from older mice showed also significantly delayed disease in the recipient NOD-Scid mice as compared with those from the corresponding wt-mice. On the other hand, IL-17/IFN-γreceptor double-deficiency significantly suppressed the development of diabetes, although the levels of insulitis were similar between single-deficient and double-deficient mice. These results indicate that IL-17/Th17 plays a significant role in the development of insulitis in pre-diabetic NOD mice and the interaction of Th1-Th17 cells contributes to diabetes development.
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