Generous donor and matching ICIS funds endow annual memorial lecture honoring Professor Jürg Tschopp whose discoveries in the area of inflammasomes and cell death advanced fundamental understanding of innate and adaptive immunity bringing new therapies to patients suffering from debilitating inflammatory diseases.
The purpose of the Jürg Tschopp Memorial Symposium is to inspire current and future generations of scientists to perform cutting edge research that can be translated to make a difference in patients’ lives in honor of Dr. Tschopp’s legacy, his ability to take fundamental discoveries at the bench into the clinic.
Of particular relevance to the cytokine society is Tschopp’s discovery of the inflammasome complex, a protein complex that coordinates the production of the inflammatory cytokines IL-1 and IL18 which propagate the inflammatory response. “In a scientific tour de force, Tschopp’s laboratory showed that the tender, swollen joints and excruciating pain associated with gout are caused by uric-acid crystals activating the inflammasome. Based on these findings, Tschopp persuaded the clinical-rheumatology group at the University of Lausanne to conduct human trials using IL1RA, to block IL1 one of the cytokines driving inflammation downstream of the inflammasome, now a treatment for gout. The results were stunning. Patients enjoyed almost immediate, dramatic and prolonged relief.” From Vishva Dixit, Genentech
OBITUARY| Cell Volume 145, Issye 4, P493-494, MAY 13, 2011, Jürg Tschopp 1951–2011, Richard A. Flavell
DOI: https://doi.org/10.1016/j.cell.2011.04.027
Nature Volume 472, page 296 (2011) Published: 13 April 2011
Jürg Tschopp (1951–2011), Vishva Dixit
https://doi.org/10.1016/j.cell.2011.04.027
Science Vol 332, issue 6030, page 679 Published May 2011
Jürg Tschopp (1951–2011), Luke A. O’Neill
Jürg Tschopp, Winner of the 2008 Louis Jeantet Prize for Medicine
JÜRG TSCHOPP is awarded the 2008 Louis-Jeantet Prize for Medicine for his pioneering work in the fields of cell death and inflammation. He uncovered the key role played in these two processes by the Fas and inflammasome protein assemblies.