2013 Fiscal Year Final Research Report
Analysis of the effector T cells in the pathogenesis of experimental autoimmune thyroid disease
| Project/Area Number |
23791060
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Endocrinology
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| Research Institution | Nagasaki University |
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Principal Investigator |
HORIE Ichiro 長崎大学, 大学病院, 助教 (30457577)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 甲状腺 / 自己免疫 / IL-17 / IFN-gamma / Th17 / Th1 / バセドウ病 / 橋本病 |
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| Research Abstract |
We hypothesized that robust induction of a single arm of effector T cells, either Th1 or Th17, might be sufficient for inducing thyroiditis in NOD-H2h4 mice. To address this hypothesis, enhanced immune responses consisting of either Th1 or Th17 were induced by anti-CD25 antibody-mediated depletion of regulatory T cells in thyroiditis-resistant IL-17 knockout or IFN-receptor KO, respectively, NOD-H2h4 mice. Depletion of Treg in IL-17 KO mice elicited antithyroglobulin autoantibodies and thyroiditis. Our findings demonstrate that a robust Th1 immune response can by itselfinduce thyroiditis in otherwise thyroiditis-resistant IL-17 KO mice. Thus, unlike Th17 cells in IFN-RKO mice, Th1 cells enhanced by Treg depletion can be sustained and induce thyroiditis.
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