| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Outline of Final Research Achievements |
Canonical NF-κB is involved in the function of intestinal epithelial cells (IECs), however; the role of noncanonical NF-κB in IECs has not been well understood. We found that intestinal M cells exhibit prominent RelB nuclear translocation, which is a marker of noncanonical NF-κB activation. Based on this we evaluated the significance of RelB in M cell development. Organoids established from RelB-deficient mouse could not give rise to M cell upon RANKL administration, suggesting the essential role of noncanonical NF-κB in M cell development. In addition, we evaluated the role of TRAF6, which is essential regulator of RANKL-RANK-mediated NF-κB activation. As we expected, TRAF6-deficient mice exhibited M cell loss in Peyer’s patches. Consistent with this, IgA responses to pathogenic bacterial infection were significantly decreased in TRAF6-deficient mice compared to control mice. Our study demonstrates that TRAF6-mediated noncanonical NF-κB is essential for M cell development.
|
