Epistatic interaction of FcgammaRIIB and Sle16 polymorphism in rheumatoid arthritis

2014 Fiscal Year Final Research Report

• Project/Area Number: 24590491
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Juntendo University
• Principal Investigator: HIROSE Sachiko 順天堂大学, 医学部, 准教授 (00127127)
• Co-Investigator(Renkei-kenkyūsha): AMANO Hirofumi 順天堂大学大学, 医学部, 准教授 (50318474)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 疾患モデル / 関節リウマチ / ループス腎炎 / 疾患感受性

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.

Free Research Field

免疫病理学