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One or more keywords matched the following properties of Greiner, Dale
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Academic Background

Dale Greiner is currently Professor of Molecular 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, joined the Department of Medicine at the University of Massachusetts as Professor in 1991 and abecame a Professor od Molecular Medicine in 2010. He became Co-Director with Dr. David Harlan of the Diabetes Center of Excellence in 2010 and the Dr. Eileen L. Berman and Stanley I. Berman Foundation Chair in Biomedical Research Professor in 2013.

To date, Dr. Greiner has co-authored more than 300 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 and the Hypersensitivity, Autoimmune, and Immune-mediated Diseases 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, 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 in collaboration with Dr. Leonard Shultz at The Jackson Laboratory. 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, because these mice readily accept human cells and tissues, we are now using them to study human regenerative medicine, immunity, human-specific infectious agents and cancer. Our studies in humanized mice have the potential to guide human clinical trials by determining the mechanisms by which therapeutic approaches such as those based on the new technology of RNAi can act directly on human immune systems, islets, and cancers in vivo, facilitating the direct translation of these agents into the clinic.

One or more keywords matched the following items that are connected to Greiner, Dale
Item TypeName
Academic Article Disruption of the Jnk2 (Mapk9) gene reduces destructive insulitis and diabetes in a mouse model of type I diabetes.
Academic Article Effects of irradiation on diabetes in the BB/Wor rat.
Academic Article Humanized mouse models to study human diseases.
Academic Article Humanized mice for immune system investigation: progress, promise and challenges.
Academic Article Recapitulation of normal and abnormal BB rat immune system development in scid mouse/rat lymphohemopoietic chimeras.
Academic Article Humanized mice for the study of type 1 diabetes and beta cell function.
Academic Article Human immune system development and rejection of human islet allografts in spontaneously diabetic NOD-Rag1null IL2rgammanull Ins2Akita mice.
Academic Article Role of host immune system in BB/Wor rat. Predisposition to diabetes resides in bone marrow.
Concept Immune System Diseases
Concept Immune System
Academic Article Human cancer growth and therapy in immunodeficient mouse models.
Academic Article Generation of Immunodeficient Mice Bearing Human Immune Systems by the Engraftment of Hematopoietic Stem Cells.
Academic Article Humanized Mouse Models of Clinical Disease.
Academic Article Humanized mouse models of immunological diseases and precision medicine.
Academic Article Modeling human T1D-associated autoimmune processes.
Academic Article Humanized mouse models for immuno-oncology research.
Academic Article NOD-scid IL2r?null mice lacking TLR4 support human immune system development and the study of human-specific innate immunity.
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  • Immune System