The comtribution of complement regularoty factor, CD46, during T cell mediated rejection in kidney allograft

2014 Fiscal Year Final Research Report

• Project/Area Number: 25893119
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Urology
• Research Institution: Osaka University
• Principal Investigator: KAKUTA Yoichi 大阪大学, 医学(系)研究科(研究院), 助教 (40710116)
• Project Period (FY): 2013-08-30 – 2015-03-31
• Keywords: 腎移植 / 拒絶反応 / 補体 / 補体制御因子

Outline of Final Research Achievements

The complement system plays a critical role in both innate and adaptive immune responses. We found locally produced complement component 3 (C3) from renal allografts and downregulation of complement regulatory factor(CRF) activated the complement system during acute cellular rejection in animal models. When anti-CRF antibody was injected, acute cellular rejection was promoted. Moreover,　We demonstrated that CD46 expression in human renal tubular cells during acute cellular rejection may influence the outcome of treatment and graft survival. Grafts from older donors may be a risk factor for decreased expression of CD46 in renal tubular cells. The clinical application of complement regulatory protein including CD46 and complement regulatory drugs is considered to have some potential for suppressing acute cellular rejection after transplantation and to improve graft outcome.

Free Research Field

腎移植