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Aldo Rossini, M.D.Academic Role: Professor
Faculty Appointment(s) In:
Other Affiliation(s):
Diabetes Research
Until recently, the function of RT6 protein was unknown. We have now demonstrated that RT6 belongs to a family of NAD glycohydrolase (NADase) enzymes which convert an important cellular metabolite, nicotinamide adenine dinucleotide (NAD), into adenosine diphosphoribose (ADPR) and nicotinamide (NIC). It is interesting to note that nicotinamide, one of the products of NAD catabolism by RT6, is currently in clinical trials as a potential drug to prevent human Type I diabetes. Transplantation provides a means to treat not only the primary defect in diabetes (the absent islets of Langerhans), but also the organs damaged through secondary complications (such as the kidney). Our laboratory has demonstrated that donor specific transfusion and treatment with anti-CD40L antibody results in permanent islet allograft survival and prolonged skin allograft survival in mice. We have also observed that this system can prolong xenografts of rat tissues in mice. Our method of tolerance induction does not cause generalized immunosuppression. Prior to clinical application of our two element protocol, the feasibility of its effectiveness is being tested in primates. Our preliminary results suggest that our approach induces permanent allograft acceptance. 
Figure LegendWe are conducting a series of interrelated experiments to investigate how tolerance may fail, resulting in autoimmune diabetes, and how tolerance may be induced so as to permit the implementation of curative organ transplantation. We are studying these two aspects of tolerance using coordinated, interactive research methods. Recent PublicationsRossini, AA, Greiner, DL, and Mordes, JP: Induction of immunological tolerance for transplantation. Physiological Reviews, 79:99-141, 1999. Potential Rotation ProjectsWe offer lab rotations for Graduate Students interested in transplantation immunology; cellular immunology. Laboratory Personnel
Academic BackgroundAldo Rossini received his MD from St. Louis University School of Medicine in 1968. He served his internship and residency at St. Louis University Group Hospitals. He then served two years at the Charleston Navy Hospital in Charleston, South Carolina. He completed a joint Endocrinology and Diabetes Fellowship at Harvard Medical School, the Peter Bent Brigham Hospital, and the Joslin Diabetes Foundation (1972-74). Between 1974 and 1978 he was appointed to faculty positions at both the Peter Bent Brigham and Joslin Diabetes Foundation. In 1978 he joined the Department of Medicine at the University of Massachusetts Medical School. Since 1982 he has served as Director of the Division of Diabetes. In 1997, he received The William and Doris Krupp Professorship of Medicine Award.
Office: Biotech2 Suite 218
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The goal of our research is to understand the mechanisms of tolerance as they apply to 1) the pathogenesis of autoimmune insulin-dependent (Type I) diabetes mellitus and 2) its cure by pancreatic islet transplantation. Type I diabetes occurs when ‘auto reactive immune cells, which are normally present but held in check by ‘suppressor’ immune cells, begin to destroy the body's insulin-producing beta cells. In the BB rat model of Type I diabetes cell surface expression of RT6 is a marker for suppressor cells. To date, RT6 is the only known marker in any species for immune cells that possess such suppressor activity.
373 Plantation Street Worcester, MA 01605