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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 Induction of islet transplantation tolerance using donor specific transfusion and anti-CD154 monoclonal antibody.
Academic Article NOD mice have a generalized defect in their response to transplantation tolerance induction.
Academic Article Virus-induced abrogation of transplantation tolerance induced by donor-specific transfusion and anti-CD154 antibody.
Academic Article Improved skin allograft tolerance induced by treatment with donor splenocytes and an extended course of anti-CD154 monoclonal antibody.
Academic Article NOD congenic mice genetically protected from autoimmune diabetes remain resistant to transplantation tolerance induction.
Academic Article Blockade of CD40-mediated signaling is sufficient for inducing islet but not skin transplantation tolerance.
Academic Article Induction of tolerance for islet transplantation for type 1 diabetes.
Academic Article Induction of immunologic tolerance for transplantation.
Academic Article Genetic separation of the transplantation tolerance and autoimmune phenotypes in NOD mice.
Academic Article Islet cell autoimmunity and transplantation tolerance: two distinct mechanisms?
Academic Article CTLA4 signals are required to optimally induce allograft tolerance with combined donor-specific transfusion and anti-CD154 monoclonal antibody treatment.
Academic Article Allogeneic hematopoietic chimerism in mice treated with sublethal myeloablation and anti-CD154 antibody: absence of graft-versus-host disease, induction of skin allograft tolerance, and prevention of recurrent autoimmunity in islet-allografted NOD/Lt mice.
Academic Article Partial versus full allogeneic hemopoietic chimerization is a preferential means to inhibit type 1 diabetes as the latter induces generalized immunosuppression.
Academic Article A novel alloantigen-specific CD8+PD1+ regulatory T cell induced by ICOS-B7h blockade in vivo.
Academic Article Type 1 IFN mediates cross-talk between innate and adaptive immunity that abrogates transplantation tolerance.
Academic Article TLR agonists abrogate co-stimulation blockade-induced mixed chimerism and transplantation tolerance.
Academic Article Depletion of the programmed death-1 receptor completely reverses established clonal anergy in CD4(+) T lymphocytes via an interleukin-2-dependent mechanism.
Academic Article Skin allograft maintenance in a new synchimeric model system of tolerance.
Academic Article Islet cell transplantation tolerance.
Academic Article Engraftment of human HSCs in nonirradiated newborn NOD-scid IL2r? null mice is enhanced by transgenic expression of membrane-bound human SCF.
Academic Article Genetic disassociation of autoimmunity and resistance to costimulation blockade-induced transplantation tolerance in nonobese diabetic mice.
Academic Article Hematopoietic chimerism and central tolerance created by peripheral-tolerance induction without myeloablative conditioning.
Academic Article Autoimmune diabetes and resistance to xenograft transplantation tolerance in NOD mice.
Academic Article Rapid quantification of naive alloreactive T cells by TNF-alpha production and correlation with allograft rejection in mice.
Academic Article Viral infection: a potent barrier to transplantation tolerance.
Academic Article Role of innate immunity in transplantation tolerance.
Academic Article T-cell activation and transplantation tolerance.
Concept Transplantation Tolerance
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