Gordon Freeman is an immunologist known for his work on the costimulatory signals that regulate T cell activation. These include identifying the PD-L1/PD-1 pathway and the immunostimulatory consequences of blocking the PD-L1/PD-1 pathway. Together with his work showing PD-L1 expression on tumor cells, this has led to the development of PD-L1/PD-1 cancer immunotherapy. He is also known for his studies on B7-1 (CD80) and B7-2 (CD86) costimulatory signals through CD28 and CTLA-4 that provided important translational insights unpinning the development of immunotherapies for cancer, autoimmune diseases, and transplant rejection. Freeman was born in New Jersey and grew up in Fort Worth, Texas. He graduated from Harvard University with an AB in Biochemistry and Molecular Biology (1973), and from Harvard University with a PhD in Microbiology and Molecular Genetics (1979) in the lab of Alice Huang. He was a postdoctoral fellow with Harvey Cantor and Lee Nadler at the Dana-Farber Cancer Institute. He joined the faculty at Harvard Medical School in 1991 and was promoted to Professor in 2015. He was listed as a Highly Cited Researcher in Immunology by Thomson Reuters in 2002 and all subsequent years and as a 2016 Citation Laureate. He received the William B. Coley Award for Distinguished Research in Tumor Immunology in 2014, the Warren Alpert Foundation Prize in 2017, the Richard V. Smalley, MD Memorial Award in 2020, and other awards for his contributions to the discovery of the PD-L1/PD-1 pathway. He has been elected to the National Academy of Sciences, the National Academy of Inventors, and is an Inaugural Fellow of the Academy of Immuno-Oncology of SITC, a Fellow of the AACR Academy and the American Academy of Arts and Sciences.

Research Interests

The Freeman lab is interested in the T cell costimulatory and coinhibitory signals that regulate the strength and duration of an immune response. The Freeman lab identified the major pathways that control the immune response by inhibiting T cell activation (PD-L1/PD-1 and B7-2/CTLA-4) or stimulating T cell activation (B7-2/CD28). Dr. Freeman discovered PD-L1 and PD-L2, and showed they were ligands for PD-1, thus defining the PD-1 pathway and the drug target: block the interaction. He showed the function of PD-1 was to inhibit immune responses and that blockade enhanced T cell activation, cytokine production and cytolysis. He showed that PD-L1 is highly expressed on many solid tumors such as breast and lung, as well as some hematologic malignancies and allows these tumors to inhibit immune attack. With Arlene Sharpe, he investigated the in vivo role of these pathways. Blockade or engagement of costimulatory and coinhibitory pathways has numerous therapeutic applications including PD-L1/PD-1 and CTLA-4 cancer immunotherapy, now FDA approved in over 25 cancer types. He has investigated additional costimulatory pathways including TIM-3/phosphatidylserine, HHLA2/KIR3DL3, CD160/HVEM, ICOS/ICOS-Ligand, and Sema4D (CD100). More recently, he has studied alternative interactions of PD-L1 with B7-1 and of PD-L2 with RGMb. These have therapeutic possibilities in autoimmunity, asthma, and cancer. In particular, the gut microbiome uses PD-L2/RGMb to regulate the immune response and blockade increases the response to cancer immunotherapy. Further work is focused on how the immune response is regulated and how this understanding can be applied to alleviate disease.

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Primary Section

Section 43: Immunology and Inflammation

Secondary Section

Section 41: Medical Genetics, Hematology, and Oncology