Research Group

  • Dr Peter Heeger, Principal Investigator
  • Dr Shuguong Yuan, Post-doctoral Fellow/Microsurgeon
  • Ms Earla Biekert, Technician


  • The Cleveland Clinic, Cleveland, USA


  • Complement Proteins regulate the Immune Responses that cause Transplant Rejection

Transplantation is the preferred therapy for end-stage organ failure, but despite significant improvements, long-term graft survival is limited, largely due to chronic immune-mediated injury to the transplanted organ. The goal of the present study is to better understand the basic mechanisms of graft rejection so as to be able to use this information to design novel therapies that will prolong graft survival. T cells and antibodies reactive to the “foreign” transplanted organ are the key mediators of the graft rejection but we presently do not fully understand how these cellular and molecular immune mediators function to destroy an organ.

Our group recently discovered that soluble proteins comprising the complement cascade and cell-surface proteins that control the activation of complement surprisingly influence the strength of T and B cell immune responses directed at the graft. This important link between elements of the innate (complement) and adaptive (T cells and B cells) immune systems has not been well studied in transplantation. We therefore propose to use a mouse model of heart transplantation, using animals with and without targeted deficiencies or overexpression of complement/complement regulatory proteins, to assess how complement and the decay accelerating factor influence T cell alloimmunity, alloantibody production, and transplant survival. In addition to providing new information that could be exploited for prevention of graft rejection, the fundamental insights derived from this work could be applied to a variety of immune-mediated processes, including the development of approaches to enhance vaccine efficacy.

Final Report