Dr. Jeffrey Bluestone

Professor, Diabetes Center and Department of Medicine, UCSF

Research

Dr. Bluestone is involved in two major areas of the application. First, he supervises Linda Vo, who is directly involved in Core B. Together, Drs. Vo and Bluestone have established the use of iPS cells to derive antigen‐specific T cells differentiated from Ezh1‐disrupted CD34+ cells. Core A will provide CD34+ cells for the group and enable Project 1 to develop novel antigen‐specific Tregs for therapeutic use. The efforts will also include technology, developed in collaboration with Alex Marson’s lab, to introduced specific T cell receptors into the TRAC (T cell receptor alpha constant) locus, replacing the endogenous TCR with the specified tumor‐specific receptor.

Finally, the Core will develop CRISPR technology to modify iPS cells to eliminate MHC and other potentially immunogenic proteins and over‐express key cloaking molecules to develop universal, off‐the‐shelf T cells for adoptive immunotherapy. Dr. Bluestone is also involved in Project 1 as the A.W. and Mary Margaret Professor in the Department of Medicine (Endocrinology) and the Director of the UCSF Hormone Research Institute. His group has researched the fundamental nature of the immune system in the pancreatic islets and recently developed technologies for isolating, expanding and using regulatory T cells in patients with T1D. As a co‐PI for the Center, Bluestone will work with Dr. Tang and others to develop tools, identify T cell receptors and build genetically engineered Tregs for therapeutic application. He will also work closely with Dr. Nolan at Stanford to use high resolution CODEX to timsTOF‐based CAPP as a platform for performing high‐dimensional examination of pancreatic tissue samples to interrogate the dynamics of the cellular and biochemical subcellular and tissue microenvironment in T1D patients. Dr. Bluestone has extensive experience working with both the UCSF and Stanford teams in multiple programs including the development of islet transplantation, Treg therapy and the use of novel molecular tools to define the pathogenesis of T1D.