| Project/Area Number |
26860755
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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 |
Collagenous pathology/Allergology
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | IgG4関連腎臓病 / IRF-1 / MRL/lprマウス / Irf1 / MRL/lpr / IgG4関連疾患 / 尿細管間質性腎炎 |
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| Outline of Final Research Achievements |
We analyzed renal pathology of lupus-prone MRL/lpr mice deficient for a transcriptional regulator, interferon regulatory factor-1(IRF-1), and compared their pathogenesis with those of human IgG4-related kidney disease (IgG4-RKD) for validation of IRF-1 KO MRL/lpr mice as a murine model for IgG4-RKD. They exhibited significant infiltrations of eosinophils, CD4-T cells, and IgG1-plasma cells in their renal tubulointerstitia from 9 weeks of age but not in their glomeruli. Furthermore, they exhibited significant Th2 polarity in their spleens and kidney-infiltrating lymphocytes. Despite the improved glomerular inflammation, they showed a high level of blood urea nitrogen and albuminuria, possibly due to their tubulointerstitial inflammatory lesions. Our results suggested that IRF-1 KO MRL/lpr mice could be conveniently used for a model for IgG4-RKD since they showed significant Th2 polarity and severe tubulointerstitial nephritis with impaired renal function.
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