My research focuses primarily on immunology and transplantation, with emphasis on the transplantation pathology of the heart, kidney, and pancreatic islets. I am particularly interested in how the acute and chronic rejection of allografts and xenograft come about. Studies involve patients and animal experimentation of heart, kidney, and pancreatic islet grafts. With expertise in these areas, I am a consultant pathologist to many investigators within the Harvard community, and to national consortia with clinical transplant programs. I am also a consultant to revisions of the classification scheme for human heart allograft biopsies. 
    Current emphasis and ongoing work includes cellular and humoral rejection in cardiac and renal transplantation. I have been able to correlate indirect immunofluorescence C4d staining with alloantibodies by retrospective and prospective analysis of the cardiac allograft biopsies. This study establishes for the first time the correlation between C4d staining and the presence of alloantibodies. This has been extended to include immunoperoxidase staining of paraffin sections to study chronic rejection in cardiac allograft patients with the goal of trying to establish a link between chronic allograft vasculopathy in human hearts and the development of alloantibodies. 
    We are also studying the progression of chronic kidney allograft rejection that comes about with development of alloantibodies. We have been able to establish that alloantibodies strongly associate with and are likely causative of the glomerulopathy of chronic humoral rejection in allografted kidneys, thereby, establishing that chronic humoral rejection develops through four stages. Ongoing studies involve the study of allograft endothelium.
    With other investigators we have established that streptozotocin affects the autoimmunity in NOD mouse (a mouse model of spontaneous diabetes). We have also established the optimal dose of streptozotocin for monkey preclinical islets transplant protocols, and have established that limiting numbers of islets can suffer a non-immunological senescence. We have established that the failure of an islet allograft was not immunologically based. With other investigators we are investigating why the knockout of certain chemokine genes affects graft rejection and ischemic injury. With investigators at the Transplantation Research Center we have shown that a complement regulatory protein, DAF, can inhibit acute humoral rejection to limiting titers of antibody.
With other investigators we are exploring dendritic cell antigen uptake, optimal protocols for tolerance induction, and  immunomodulatory effects stem cells in mice.

Current emphasis is the analysis of gene expression using SAS, python, and machine learning.