Jeffrey Bluestone

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Jeffrey Bluestone
Alma materRutgers University, Weill Cornell Graduate School of Medical Sciences
Known forImmune tolerance in Autoimmunity, Organ Transplantation and Cancer
Scientific career
InstitutionsUniversity of California, San Francisco
Doctoral advisorCarlos Lopez
Other academic advisorsDavid Sachs

Jeffrey A. Bluestone is a Professor of Metabolism and Endocrinology and the Director of the Hormone Research Institute in the Diabetes Center at the University of California, San Francisco. He earned his B.S. in Biology and M.S. in Microbiology from Rutgers University in 1974 and 1977 respectively and his Ph.D. in Immunology from Weill Cornell Graduate School of Medical Sciences in 1980 with Carlos Lopez. His research is focused on understanding T cell activation and autoimmunity.[1] He also serves as the President and CEO of the Parker Institute for Cancer Immunotherapy[2]


He started his career as an investigator in the immunology branch of the National Cancer Institute. From 1987 to 2000, he was a professor in the department of pathology at University of Chicago and was the chairman of the Committee on Immunology. From 1995 to 2000, he was the director of the Ben May Institute for Cancer Research. In 2000, he moved to the University of California, San Francisco to direct the UCSF Diabetes Center and metabolic research unit. Bluestone heads the Immune Tolerance Network, a consortium of over 1000 scientists to focus efforts on the development of immune tolerance therapies.[3] From 2010 to 2015, he was the Executive Vice Chancellor and Provost of University of California, San Francisco. As the Provost, he set up a lot of the academic industry collaborations currently in place at UCSF.[4] He is a member of the National Academy of Medicine and a Fellow of the American Academy of Arts and Sciences He is a member of the Editorial Board for Immunity.


The Bluestone group is particularly focused on studying the role of T cell receptors on Regulatory T cells ("Tregs"). In the early 90s, he identified the role of CD28 and its interaction with CTLA-4 [5] The development of soluble receptors of CTLA-4 led to the development of the drugs abatacept and later belatacept.[6] Further work with James P. Allison to target CTLA-4 resulted in the development of immune checkpoint therapies also known as immunotherapy. This led to the clinical development of ipilimumab (Yervoy™), which was approved in 2011 by the FDA for the treatment of metastatic melanoma. Their current work on understanding Tregs may lead to further developments to treat Type 1 Diabetes.[7]


  1. ^ "Jeffrey Bluestone". UCSF. Retrieved 4 August 2016.
  2. ^ Farley, Pete (12 April 2016). "UCSF Immunologist to Head New Parker Institute for Cancer Immunotherapy". UC San Francisco. UCSF News. Retrieved 4 August 2016.
  3. ^ "Jeffrey Bluestone". Brehm Coalition. Archived from the original on 2016-08-16. Retrieved 4 August 2016.
  4. ^ Timmerman, Luke (10 March 2011). "Q&A: UCSF's Jeff Bluestone on the Tricky Balancing Act Between Academia and Industry | Xconomy". Xconomy. Retrieved 4 August 2016.
  5. ^ Walunas, TL; Lenschow, DJ; Bakker, CY; Linsley, PS; Freeman, GJ; Green, JM; Thompson, CB; Bluestone, JA (August 1994). "CTLA-4 can function as a negative regulator of T cell activation". Immunity. 1 (5): 405–13. doi:10.1016/1074-7613(94)90071-x. PMID 7882171.
  6. ^ Levisetti, MG; Padrid, PA; Szot, GL; Mittal, N; Meehan, SM; Wardrip, CL; Gray, GS; Bruce, DS; Thistlethwaite JR, Jr; Bluestone, JA (1 December 1997). "Immunosuppressive effects of human CTLA4Ig in a non-human primate model of allogeneic pancreatic islet transplantation". Journal of Immunology. 159 (11): 5187–91. PMID 9548454.
  7. ^ Conovo, Susan (26 June 2002). "Stopping Diabetes". (11). In Vivo. Retrieved 4 August 2016.

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