“I am excited about all of the discoveries that we and our colleagues around the world are making about the immune system and what is causing type 1 diabetes.”

Alberto Pugliese, M.D.

Alberto Pugliese, M.D., is The J. Enloe and Eugenia J. Dodson Chair in Diabetes Research, Professor of Medicine, Microbiology and Immunology and Deputy Director of Immune Tolerance at the Diabetes Research Institute.

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Dr. Pugliese, who joined the DRI in 1994, is dedicated to advancing type 1 diabetes research through scientific excellence, open collaboration, and the training of new investigators. For the last 25 years, he has studied type 1 diabetes from the preclinical period to the clinical diagnosis, and afterwards, in the setting of transplantation.

His work examines the role of genetic and immunological factors that lead to, or protect against, the development of type 1 diabetes. His studies have led to improved understanding of genetic and cellular mechanisms that regulate immunological self-tolerance (acceptance) specifically to molecules targeted in diabetes. Dr. Pugliese’s research has provided seminal contributions in type 1 diabetes genetics, immunology, pathology, and clinical trials. Selected contributions include:

1) The discovery that insulin and other molecules targeted by autoimmune responses are expressed in the thymus. This highlighted an unknown role for the thymus in establishing immunological self-tolerance for molecules with tissue-related expression.

2) The discovery that not all individuals with autoimmune responses associated with type 1 diabetes are destined to develop clinical disease. His research identified that certain genetic variants afford protection from type 1 diabetes, despite ongoing autoimmune responses, which are now included in the main exclusion criteria for prevention trials.

3) The discovery that chronic immunosuppression does not always protect pancreas transplant recipients from recurrent diabetes. This finding challenged the long-held belief that immunosuppression that prevents rejection also contains autoimmunity, and provided evidence for the extreme chronicity of islet autoimmunity.

4) In collaborative studies, the definition of critical mechanisms by which interleukin-2 may be used as a therapeutic agent in type 1 diabetes. These studies showed that at a low dose, interleukin-2 selectively promotes immune regulation without activating immune responses. This observation lays the foundation for a clinical trial to determine if this therapy can regulate autoimmunity without inducing generalized immunosuppression.

Since 2001, Dr. Pugliese has been a steering committee member of the Type 1 Diabetes TrialNet (www.diabetestrialnet.org), a National Institutes of Health-funded clinical trial network, for which he has chaired several committees and initiatives. He is also Executive Co-Director of the JDRF Network for Pancreatic Organ Donors (www.JDRFnPOD.org), a collaborative project that recovers tissues from organ donors with type 1 diabetes and distributes these samples to investigators worldwide to support a comprehensive understanding of the human disease.

Dr. Pugliese is indeed a champion for team-science approaches, which has been recognized by the Helmsley Charitable Trust with the George S. Eisenbarth nPOD Award for Team Science.

Dr. Pugliese has served on research grant review committees of the National Institutes of Health, the JDRF, and chaired the American Diabetes Association’s Grant Review Panel.

His research has been published in major international journals including Nature Genetics, Nature Immunology, Journal of Clinical Investigation, Lancet, among other prestigious, peer-reviewed journals.

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