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Stefan Feske, MD

Stefan Feske, MD

Picture of Stefan Feske, MD

Stefan Feske is an Associate Professor in the Department of Pathology's Experimental Pathology Program.

Biographical Sketch

Stefan Feske studied medicine at the universities of Hamburg and Freiburg in Germany from which he graduated summa cum laude with an MD degree. For his research thesis on a signal transduction defect in T lymphocytes as the cause for severe combined immunodeficiency he received the Ludwig-Heilmeyer Award of the University of Freiburg.

Stefan did his residency in internal medicine in the Division of Rheumatology and Clinical Immunology at the University Hospital Freiburg under the guidance of Hans-Hartmut Peter while conducting a brief postdoctoral research period in the laboratory of Klaus Eichmann at the Max-Planck Institute for Immunobiology in Freiburg.

For his postdoctoral studies, Stefan joined the laboratory of Anjana Rao at the Immune Disease Instutute (formerly known as Center for Blood Research) at Harvard Medical School. There he identified the abnormal activation of the transcription factor NFAT in T cells from immunodeficient patients and identified a defect in Ca2+ influx and the function of the CRAC Ca2+ channel as the underlying cause of disease in these patients. In collaboration with the lab of Louis M. Staudt at the NIH he used the then novel technology of DNA microarrays to characterize the role of Ca2+ influx for gene expression in lymphocytes.

As a postdoc and instructor at Harvard Medical School, Stefan embarked on several years of investigations in order to track down the gene encoding the CRAC channel and causing immunodeficiency. The molecular nature of this channel had been mysterious since its initial description in the late 1980s. That search ended when Stefan and his colleague Yousang Gwack in Anjana Rao's lab discovered ORAI1 as a new gene and critical component of the CRAC channel by positional cloning in patient cells and a functional RNAi screen in Drosophila cells. In collaboration with Murali Prakriya from Northwestern University and Richard S. Lewis from Stanford University, Stefan and colleagues were able to show that ORAI1 is a pore forming subunit of the CRAC channel.

In the meantime Stefan was promoted to assistant professor of Pediatrics at Harvard Medical School, where he soon became interested in the role of ORAI1 and STIM1, a protein that had been identified as an important regulator of CRAC channel function just one year before the discovery of ORAI1, in immune responses in vivo. For his studies on immunodeficiency and the discovery of ORAI1 as an important regulator of T cell activation, Stefan received the prestigious Georges-Koehler Award from the German Immunology Society in 2007.

In 2007, Stefan accepted a faculty position as assistant professor in the Department of Pathology at NYU School of Medicine, where he was promoted to associate professor in 2012. His research is focused on the mechanisms regulating ORAI and STIM protein function and the role of CRAC channels in immune responses. His lab investigates how calcium influx through CRAC channels shapes immunity to infection, autoimmunity and antitumor immune responses using gene-targeted mice lacking expression of functional Orai and Stim genes. The Feske Lab also continues to characterize inherited immunodeficiencies due to mutations in STIM and ORAI genes, which are the cause of a unique novel disease termed CRAC channelopathy.   

Stefan co-directs the Pathobiology graduate training program at NYU and teaches immunology courses at the Medical School. He is also a scientific co-founder and advisor to Calcimedica, a biotechnology company based in San Diego that tries to develop CRAC channel inhibitors for the treatment of immune diseases.