Bruce Beutler, MD

Bruce Beutler, MD   discovered an important family of receptors that allow mammals to sense infections when they occur, triggering a powerful inflammatory response. For this work he received the 2011 Nobel Prize in Physiology or Medicine.

Dr. Beutler received his undergraduate degree from the University of California at San Diego in 1976, and his MD degree from the University of Chicago in 1981. After two years of residency at the University of Texas Southwestern Medical Center, he became a postdoctoral fellow and then an Assistant Professor at the Rockefeller University (1983-1986), where he isolated mouse tumor necrosis factor (TNF) and was the first to recognize TNF as a key executor of the inflammatory response. Returning to Dallas in 1986 as an HHMI investigator, he designed recombinant inhibitors of TNF that are widely used in the treatment of rheumatoid arthritis and other inflammatory diseases. He also used TNF as a biological endpoint in order to identify the receptor for bacterial lipopolysaccharide (LPS). This he achieved by positionally cloning the Lps mutation of mice, known to prevent all biological responses to LPS, including TNF production. He thus concluded that Toll-like receptor 4 (TLR4) acts as the signaling core of the LPS receptor and proposed that other TLRs might also recognize conserved molecular signatures of infection.

Moving in 2000 to the Scripps Research Institute, Dr. Beutler developed the largest mouse mutagenesis program in the world, and applied a forward genetic approach to decipher the signaling pathways activated by TLRs. He also identified many other molecules with non-redundant function in the immune response.  Returning to UT Southwestern in 2011, he developed a means of instantly identifying mutations responsible for both quantitative and qualitative phenotypes.  This allowed rapid discovery of many new components of the immune system.