| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Outline of Final Research Achievements |
Transcription factor MafB is specifically expressed in macrophages in hematopoietic cells. During the adult stage, both Mafb-deficient fetal liver cells that were transplanted into recipient mice and macrophage-specific Mafb conditional knock-out mice exhibited autoimmune phenotypes. Macrophage efferocytosis (apoptotic cells uptake) is important for inhibiting autoimmune disease. The efferocytosis ability of Mafb-deficient macrophages was strongly reduced. The expression of complement component-1q (C1q), which is known as the first protein in the classical complement pathway and for mediating efferocytosis, was reduced in Mafb-null macrophages. The promoter analysis of C1q genes showed that MafB directly regulates C1qa, C1qb, and C1qc promoter. Consistent with this result, the classical pathway was also decreased in Mafb-deficient mice analyzed by hemolysis assay. These results suggest that MafB primarily regulates C1q genes.
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