lecture:Regulatory T cells in Transplantation Tolerance Induction―New concept for allograft acceptance

   

题目:Regulatory T cells in Transplantation Tolerance Induction—New concept for allograft acceptance
报告人:XIAO-KANG LI, M.D., D.M.Sc. (Ph.D.)
Head & Senior Research Scientist,Laboratory of Transplantation Immunology,National Research Institute for Child Health and Development, Tokyo,JAPAN
主持人:韩晶岩 (中西医结合教研室,微循环研究中心)
时间:2007年11月8日(周4)15:00-16:00
地点:基础医学院生化楼3楼会议室
(用中文报告)
 
摘要:Induction and maintenance of peripheral tolerance are important mechanisms for the balance of the immune system. Growing evidence indicates that the CD4+CD25+ regulatory T (Treg) cells play a central role in the suppression of autoimmunity, inflammation and allograft rejection. However, the underlying mechanism of their functions remains mostly elusive and many studies suggest that the Treg cells have proven difficult to grow, expand and clone in vitro and in vivo. Therefore, the investigations of the novel molecular and/or pathway for understanding their regulatory functions and therapeutic agents that are capable of enhancement the number and activity of this T cell subset are highly desirable. The use of the multiple animal transplantation models has not only improved our understanding of tolerance induction, but also contributed to new concepts of treatment strategies involving the use of regulatory T cells. The present report summarizes 1) our current knowledge of regulatory T cells and their involvement in transplantation tolerance induction; 2) a fundamental role for the blockade of PD-1/PD-L1 pathway abrogated Treg cells, mediated-immune regulation in vitro and tolerance induction in vivo, using a well-characterized SCID and Rag-2/KO mice T cell transfer model; 3) using supCD28 mAb to preferentially expand Treg cells in vivo and maintain not only their phenotype but also their potent regulatory functions, represent a major advance towards the therapeutic use of these cells as cellular therapy for treatment allograft rejection and GvHD.