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, NIH

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 - 2010             Director, Immune Tolerance Network

2000 - Pres.             A. W. and Mary Margaret Clausen Distinguished Professor, University of
                                California, San Francisco, CA

2000 - 2010             Director, Diabetes Center, the Metabolic Research Unit and the Hormone
                                Research Institute

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

2010 - 2015             Executive Vice Chancellor and Provost, University of California San Francisco

2010 - Pres.             Director, Hormone Research Institute 


Lab Member Since: 
2000 - 2016
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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