Academic Background

Dale Greiner is currently Professor of Medicine at the University of Massachusetts Medical School. His research focuses on three areas: transplantation, autoimmunity, and the use of humanized mice to study human diseases and infections. Dr. Greiner graduated from the University of Iowa with a Bachelor of Science degree and Medical Technology degree in 1974 and with a Doctor of Philosophy degree in 1978. He did postdoctoral fellowships at the University of Pittsburgh and at the University of Connecticut Health Center in Farmington, CT. He was appointed Assistant Professor at UConn in 1983, Associate Professor in 1989, and joined the Department of Medicine at the University of Massachusetts as Professor in 1991.

To date, Dr. Greiner has co-authored more than 250 publications. He has served as a member of the editorial board of Diabetes, and as a regular member of the National Institutes of Health Immunology Sciences Study Section. He has served as chair of the Veterans Administration Immunology Review Subcommittee B and has served as chair of many ad hoc NIH and JDRF study sections. He has also served as Chair of the Medical Science Review Committee for the Juvenile Diabetes Research Foundation, International. He has also served as Chairman of the American Diabetes Association Scientific Sessions Committee, Program Chair of the American Diabetes Association Council on Immunology, Immunogenetics and Transplantation, and Council Chair, American Diabetes Association Council on Immunology, Immunogenetics and Transplantation.

Dr. Greiner has received numerous awards for his research, including the A.J. Julian Scholarship for Academic Excellence, the Basil O'Connor Scholar Research Award from the March of Dimes, and the Kayla and Gerald Grodsky and David Rumbough Awards from the Juvenile Diabetes Research Foundation, Int.   

Transplantation tolerance and autoimmune diabetes

Our major area of investigation is to understand the etiology and pathogenesis of autoimmune type 1 diabetes mellitus (T1D). Our approach focuses on two main areas, the understanding of the pathogenesis of type 1 diabetes so as to formulate means to prevent or reverse the disease, and the cure of those who are diabetic by induction of transplantation tolerance to islets of Langerhans. Over 25 years ago, we and others accomplished these goals in spontaneously diabetic mouse and rat models of T1D, but these accomplishments have not yet been successfully translated to humans. We believe there are two major obstacles that prevent the achievement of these goals in humans: 1) Lack of understanding of the biology of how human insulin-secreting beta cells die during the development of T1D. 2) Lack of understanding of how a human immune system mediates the destruction of human beta cells in vivo. Our laboratory is focusing on the development of “humanized” mice to study human T1D. We have developed unique strains of mice that can be engrafted with functional human cells and tissues, including human islets and human immune systems. We are now using these mice to understand how human beta cells resist killing by a human autoimmune system in vivo, how human beta cells replicate and regenerate in vivo, how human autoreactive cells develop in a human diabetes-susceptible immune system, and how a human immune system targets and kills beta cells in vivo. These approaches are allowing us to understand and dissect mechanisms important in human T1D that cannot be studied directly in humans. Moreover, our studies in humanized mice have the potential to guide human clinical trials in T1D by determining the mechanisms by which therapeutic approaches such as those based on the new technology of RNAi can act directly on human beta cells and human immune systems in vivo, facilitating the direct translation of these agents into the clinic.