The focus of the Katz Lab is to understand the role of T cells in allo- and auto-immunity. Our lab works in the area of autoimmune diabetes (Type 1 Diabetes, T1D) and multiple sclerosis (MS). We use mouse models to investigate the role of T cells and antigen presenting cells (APC) on the etiology, development and treatment of these autoimmune disorders. In addition, we study allogeneic solid organ rejection using heterotopic heart allografts.
T1D is best modeled in the non-obese diabetic (NOD) mouse model. This model allows us to study specific aspects of T1D using genetic, epigenetic and molecular and cellular immunology methods. Our lab undertakes detailed molecular studies of auto-reactive T cell development and activation and their interaction with self-antigen and APC in eliciting spontaneous T1D in the NOD mouse. In addition, we have studies ongoing to assess specific aspects of T cell peripheral tolerance in the context of T1D reversal and islet transplantation.
MS is characterized by a progressive or relapsing-remitting course of immune-mediated demyelination of nervous tissue in the CNS and brain. It is well modeled the mouse using an inducible model known as experimental autoimmune encephalomyelitis (EAE), in which defined myelin-associated antigens and antigenic peptides are used to elicit either progressive of relapsing-remitting forms of the disease. In the lab we focus on the regulation of auto-reactive T cells and their targeted elimination in pre-clinical therapeutic models.
The role of T cells in acute and chronic allograft rejection is not fully understood. Our lab studies the effects of major and minor histocompatibility differences in donor solid organs and recipients as they relate to solid organ rejection. To do this we undertake studies in mice using a heterotopic heart allograft transplant model, as well as studies using pancreatic islet and skin grafts.