Jeff Bluestone


1982 – 1986             Laboratory Leader, Senior Staff Fellow, Transplantation Biology Section,   

   Immunology Branch, NCI, NIH

1986 – 1987             Senior Investigator, Transplantation Biology Section, Immunology Branch, NCI,


1987 – 1991             Associate Professor, 1991 – 2000 Professor, Ben May Institute, Department of

   Pathology and the Committee on Immunology, University of Chicago and

   Chairman, COI

1995 – 2000             Director, Ben May Institute for Cancer Research

1999                         Director, Immune Tolerance Network

2000                         A. W. and Mary Margaret Clausen Distinguished Professor, University of

   California, San Francisco, CA and Director, Diabetes Center, the Metabolic

   Research Unit and the Hormone Research Institute

2008                         Interim Associate Vice Chancellor of Research, University of California San


2010                         Executive Vice Chancellor and Provost, University of California San Francisco

2010                         Director, Hormone Research Institute 


Lab Member Since: 
My Project: 

My research over the past 25 years has focused on understanding the basic processes that control T cell activation and immune tolerance in autoimmunity. Specifically, my work has centered on understanding and altering the positive signals delivered by the autoantigen-specific T cells and secondary, so-called co-stimulatory signals, or engaging the negative regulatory events that control T cell activation. We have developed soluble receptor antagonists; monoclonal antibodies and animals deficient in individual members of these pathways to define their individual roles in transplant rejection and autoimmunity including a special emphasis on a specialized subset of T cells termed “regulatory T cells” (Treg) that control fundamental aspect of immune homeostasis. The insights gained from these studies help in the development of a new generation of tolerogenic drugs that will "turn off" selected parts of the immune system, leaving the disease-fighting capabilities intact. One specific example was our role in the study of CD28 co-stimulation in the early 1990’s up through today. In collaboration with Bristol Myers Squib, we were the first to demonstrate that the soluble CD28 antagonist, CTLA4Ig, could block graft rejection and lead to tolerance. This study was instrumental in the development of the agent as a therapeutic drug in Psoriasis and now kidney transplantation. Finally, we have created comprehensive research and clinical programs aimed at producing rapid clinical advances in the use of therapies, such as CTLA-4Ig and Tregs to block and reverse immunologic diseases. These basic and translational research experiences positions us to be able to carry out the proposed studies.

Email Address: 

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