| Project/Area Number |
21890204
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
SEKINE Hideharu Fukushima Medical University, 医学部, 講師 (40363759)
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| Research Collaborator |
GARY GILKESON 米国サウスカロライナ州立医科大学, 教授
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2010: ¥1,235,000 (Direct Cost: ¥950,000、Indirect Cost: ¥285,000)
Fiscal Year 2009: ¥1,365,000 (Direct Cost: ¥1,050,000、Indirect Cost: ¥315,000)
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| Keywords | 全身性エリテマトーデス / ループス腎炎 / インターフェロン調節因子4 / CD4陽性T細胞 / Th1 / Th17 / CD4性T細胞 |
|---|
| Research Abstract |
Lupus-prone MRL/lpr mice, that lack interferon regulatory factor 4 (Irf4-/-MRL/lpr), develop cellular proliferative glomerulonephritis with significantly increased numbers of splenic CD4+ T cells, despite lack of antibody production and immune complex (IC) formation. To investigate the underlying mechanisms of the development of nephritis in these mice, CD4+ T cells proliferating in their spleen were analyzed. Compared to controls, Irf4-/-MRL/lpr had significantly increased numbers of IFN-γ producing Th1-type cells, and significantly increased numbers of CD62L+/CD44+ memory CD4+ T cells and CD62L-/CD44+ effector CD4+ T cells. Similar results were observed in Irf4-/-NZM2410 mice, another murine lupus model. These results suggest that Irf4 associate with the development of IFN-γ producing memory and effector Th1 cells, and the association of these cells with the development of non-IC-dependent lupus-like glomerulonephritis observed in Irf4-deficient murine models of human SLE.
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