Due to a limited supply, we are unable to accept phone calls to schedule COVID-19 vaccinations.
For the most up-to-date information, please check our COVID-19 Vaccination Website.
Associate Professor
Professor, Microbiology and Immunology
and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University
T cell-mediated immunity is a double-edge sword. T-cell immune response is clearly important for protecting the host from infections and tumors, but it also causes inflammatory disorders, such as autoimmune diseases and rejection of allogeneic grafts. Existing methods that induce pan-immunosuppression lack the efficacy to control T cell-mediated inflammation disorders. For example, although standard therapy that typically includes steroids could reduce acute rejection of allografts in patients, it fails to effectively inhibit chronic allograft rejection that becomes a leading cause of graft failure. In addition, pan-immunosuppression increases the risk of infection and causes other adverse effects. Novel approaches are urgently needed.
A major goal of our research program is to understand the molecular mechanisms regulating allogeneic T cell responses and their-mediated tissue injury (such as graftversus- host disease (GVHD), a life-threatening complication after allogeneic bone marrow transplantation). This includes analysis of effector T cell development and functional activities of effector T cells that culminate in tissue inflammation. These studies are performed primarily in mouse models of allogeneic bone marrow transplantation. One emphasis is placed on defining the role of Ezh2 (which is a key component of polycomb repressive complex 2 and histone methyltransferase) in antigen-driven T cells. Another one is investigating the role of Notch ligands and inflammatory dendritic cells (i-DCs) in immune responses. We have recently established the beneficial effects of modulating alloimmunity by targeting Ezh2 and Notch signaling pathway on preventing T cell-mediated GVHD. Results from these studies will lead to new strategies to prevent and treat alloimmune inflammation and other T cell-mediated inflammatory disorders in a broad context. Several ongoing projects in our lab include:
Department of Microbiology and Immunology, Lewis Katz School of Medicine, Temple University
Research at Fox Chase Cancer Center includes faculty from throughout Temple Health and Temple University, including the Temple School of Engineering, Temple School of Pharmacy and the Lewis Katz School of Medicine.
Department of Microbiology and Immunology, Lewis Katz School of Medicine, Temple University
Research at Fox Chase Cancer Center includes faculty from throughout Temple Health and Temple University, including the Temple School of Engineering, Temple School of Pharmacy and the Lewis Katz School of Medicine.
Associate Professor
Professor, Microbiology and Immunology
and Fels Institute for Cancer Research and Molecular Biology, Lewis Katz School of Medicine, Temple University
T cell-mediated immunity is a double-edge sword. T-cell immune response is clearly important for protecting the host from infections and tumors, but it also causes inflammatory disorders, such as autoimmune diseases and rejection of allogeneic grafts. Existing methods that induce pan-immunosuppression lack the efficacy to control T cell-mediated inflammation disorders. For example, although standard therapy that typically includes steroids could reduce acute rejection of allografts in patients, it fails to effectively inhibit chronic allograft rejection that becomes a leading cause of graft failure. In addition, pan-immunosuppression increases the risk of infection and causes other adverse effects. Novel approaches are urgently needed.
A major goal of our research program is to understand the molecular mechanisms regulating allogeneic T cell responses and their-mediated tissue injury (such as graftversus- host disease (GVHD), a life-threatening complication after allogeneic bone marrow transplantation). This includes analysis of effector T cell development and functional activities of effector T cells that culminate in tissue inflammation. These studies are performed primarily in mouse models of allogeneic bone marrow transplantation. One emphasis is placed on defining the role of Ezh2 (which is a key component of polycomb repressive complex 2 and histone methyltransferase) in antigen-driven T cells. Another one is investigating the role of Notch ligands and inflammatory dendritic cells (i-DCs) in immune responses. We have recently established the beneficial effects of modulating alloimmunity by targeting Ezh2 and Notch signaling pathway on preventing T cell-mediated GVHD. Results from these studies will lead to new strategies to prevent and treat alloimmune inflammation and other T cell-mediated inflammatory disorders in a broad context. Several ongoing projects in our lab include: