| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Outline of Final Research Achievements |
The aim of this study is to clarify the role of M2 macrophages (Mφ) in lupus nephritis (LN). M2 Mφ predominantly infiltrated into the glomeruli of active LN and the number of M2 Mφ was correlated with the amounts of proteinuria. Unlike usual phenotype of M2 Mφ, HO-1 expression was low in those glomerular M2 Mφ. Stimulation of human M2 Mφ derived from monocytes by type Ⅰ interferons induced a decrease in HO-1 expression and increases in the expression of Bach1, the repressor of HO-1, as well as the expression of IL-6. Bach1-deficient LN model mice showed longer survival and reduction of urine protein, compared to the wild type. Promoted differentiation into M2 Mφ and high HO-1 expression in kidney, which occurred in Bach1-deficient mice, contributed somewhat to the favorable outcome. The inhibition of Bach1 is promising therapeutic target of LN to restore anti-inflammatory function of M2 Mφ via upregulation of HO-1.
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