Maki Nakayama

The primary focus of Dr. Nakayama’s laboratory is to elucidate the mechanism by which anti-islet autoimmunity causing type 1 diabetes (T1D) is initiated, from the point of view of the tri-molecular complex consisting of antigen, major histocompatibility complex (MHC), and T cell receptor (TCR) that could be a key component for the development of T1D. One of current major goals is to identify antigen specificity of T cells infiltrating pancreatic islets of T1D patients and to illustrate whether and how antigen specificity determines T cell fate.

Dr. Nakayama and her colleagues recently identified that proinsulin peptides including the insulin B:9-23 peptide, which has been demonstrated as an essential autoantigen for the T1D development in an animal model, are the target antigen for islet-infiltrating T cells in multiple T1D patients. In addition, they pursue the potential of TCR sequences to be used as T cell biomarker to predict the T1D development as well as recurrence of hyperglycemia after the pancreas transplantation or clinical therapeutic trials. The ultimate goal of Dr. Nakayama’s laboratory is to develop robust antigen-based immunodiagnostic tools as well as immunotherapy to prevent and cure T1D.