Lewis L. Lanier
University of California, San Francisco
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Primary Section: 43, Immunology and Inflammation Membership Type:
Member
(elected 2010)
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Biosketch
Lewis L. Lanier is an American Cancer Society Professor and J. Michael Bishop MD Distinguished Professor Emeritus at University of California San Francisco. Dr. Lanier received his B.S. in Biology from Virginia Tech and Ph.D. in Microbiology and Immunology from UNC – Chapel Hill. After postdoctoral studies, he joined the R&D Department at the Becton Dickinson Monoclonal Center, advancing to Associate Director. In 1990, he joined the DNAX Research Institute, where he advanced to Director of Immunobiology, and in 1999 joined the faculty of UCSF. His research group studies Natural Killer cells, which recognize and eliminate cells that have become transformed or infected by viruses. In recognition of his contributions he was awarded the William B. Coley Award for Distinguished Research in Basic Tumor Immunology from the Cancer Research Institute (2002), received the Rose Payne Award for contributions to the field of Immunogenetics by the American Society for Histocompatibility and Immunogenetics (2005), was elected to the US National Academy of Sciences (2010), and the American Academy of Arts and Sciences (2011). He served as President of the American Association of Immunologists (2006-2007), received the AAI Excellence in Mentoring Award in 2017, and awarded the AAI Lifetime Achievement Award in 2023.
Research Interests
Natural killer (NK) cells are a type of white blood cell that provides protection against microbial pathogens and tumors. Since the early 1980's, our lab has investigated how NK cells distinguish between normal healthy cells and cells that are transformed or infected with viruses. NK cells express a diverse array of inhibitory and activating receptors on their cells surface that bind to ligands expressed on the cell surface of potential target cells. When encountering healthy cells, signals transmitted by inhibitory NK receptors dominate and prevent autoimmunity, whereas the loss of ligands for the inhibitory receptors or the upregulation of ligands for the activating NK receptors on infected or transformed cells allows NK cells to kill these abnormal cells and secrete cytokine that influence the subsequent response by T cells and B cells.
