Research Group

  • Dr. Hamid Rabb, Principal Investigator
  • Dr. Lorraine Racusen, Consultant
  • Dr. Peter Heeger, Consultant
  • Dr. Sam Mohapatra, Consultant


  • Johns Hopkins University School of Medicine, Baltimore, USA


  • Mechanisms of T Cell Modulation of Renal Ischemia Reperfusion Injury

Kidney ischemia is the main cause of the initial poor function of an organ transplant. Kidney ischemia predisposes to acute rejection, which in turn predisposes to chronic rejection - the major long-term cause of graft loss. There is no specific treatment for kidney ischemia. Recently, we and others have identified that the circulating T cell is an important mediator of kidney ischemic damage. This is somewhat of a surprise finding, because the T cell is known to be important in rejection, but not in organ procurement injury. The observation that the T cell is a modulator of kidney ischemia has now been well verified in experimental models. However, the underlying mechanism are unknown. We therefore propose to begin to elucidate these underlying mechanisms for this. Based on our preliminary data using a mouse model of kidney ischemia, we hypothesize that a major subset of T cells, called Th1, functionally mediates the T-cell-mediated kidney injury, and that T-cell-mediated injury requires engagement of the T cell receptor on its surface.

We plan to test this hypothesis using an established mouse model of kidney ischemia, various strains of generated mutant mice, sensitive measures of kidney function and molecular and cellular detection techniques. Our results will have implications towards the understanding of organ procurement injury and may help lead to new therapies. In addition, given the novel focus of our proposal, our results will also extend and challenge our basic understanding of the immune system.