A novel therapeutic strategy for sepsis with re-activating T cells in the elderly
| Project/Area Number |
25861735
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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 |
Emergency medicine
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| Research Institution | Tokai University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 老化 / 免疫抑制 / 敗血症 / IL-15 / SOCS1 / 免疫 / T細胞 |
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| Outline of Final Research Achievements |
Aging induces T cell exhaustion, leading to immunosuppression in sepsis. Interleukin 15 (IL-15) is a pleiotropic anti-apoptotic cytokine that promotes activation and proliferation of CD8+ T and natural killer (NK) cell. We examined whether IL-15 can ameliorate age-related exhaustion of CD8+ T cells and NK cells and improves survival rate in aged septic mice. In Peripheral blood mononuclear cells culture, IL-15 dose-dependently reversed impaired activation, including CD25 expression,Interferon-γ(IFN-γ) production,IL-15 also prevented sepsis- induced apoptosis of CD8+ T and NK cells with enhancing IFN-γ production in aged mice. Finally, IL-15 decreased bacterial load after sepsis, leading to the improvement of survival in aged mice .IL-15 decreases expression of suppressor of cytokine signaling 1(SOCS1) was decreased in CD8+ T cells from the aged septic mice. These result suggest us that SOCS1 might be a new therapeutic target for sepsis in the elderly.
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Report
(3 results)
Research Products
(16 results)
