| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
FcγRIIB is expressed on B cells and a wide variety of immune cells, and negatively controls function of these cells. In the present studies, we examined whether the lack of FcγRIIB expression leads an aberrant activation of immune cells and the development of autoimmune diseases, by establishing FcγRIIB-deficient B6 congenic strains. The result suggested that the epistatic interaction between Fcgr2b null-mutation and autoimmune-type 129-derived polymorphic gene(s) in Sle16 region located in the distal of Fcgr2b gene contributes to the RA susceptibility. Identification of the susceptibility gene(s) for RA is of paramount importance to shed light on the genetic mechanisms that control RA in humans.
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