Professor of Medicine
University of Massachusetts Medical School
Dr. Fitzgerald received her B.Sc. in Biochemistry in 1995 from University College Cork, Ireland, and her Ph.D. in 1999 from the laboratory of Professor Luke Oâ€™Neill in Trinity College Dublin, Ireland. From 1999 to 2002, she was a post-doctoral fellow in the Department of Biochemistry at Trinity College Dublin. Dr. Fitzgerald joined the Division of Infectious Disease at the University of Massachusetts Medical School as a recipient of a Wellcome Trust International Award in 2001. In 2004 she joined the Faculty as an Assistant Professor. She is currently Professor of Medicine and Director of the Program in Innate Immunity.
Research in the Fitzgerald laboratory is focused on all things related to innate immunity and the inflammatory process, with signal transduction and gene regulation being her particular area of expertise. Active research areas include: (1) biology and role of inflammasomes in anti-microbial immunity (2) cytosolic nucleic acid recognition systems in anti-viral defense and autoimmune disease, (3) long non-coding RNAs in the immune system and (4) innate immunity to Malaria. Enabling these studies, her research spans the disciplines of immunology, cell and molecular biology, biochemistry and genetics.
Dr. Fitzgerald entered the field of immunology by discovering Mal/TIRAP, a central adapter in TLR4 signaling. Since then, she has discovered TRAM, an adapter molecule important downstream of TLR4 in controlling interferon production. Since starting her own lab at UMASS, she has made multiple discoveries that have continued to impact our understanding of host-pathogen interactions. These include the discovery of TBK1/IKKe responsible for the activation of IRF3 and IRF7. Dr. Fitzgerald has also made major contributions to our understanding of the inflammasome where she identified the AIM2 inflammasome important in host-defense to viruses and bacteria. Recent studies have advanced our understanding of how Gram negative bacteria are detected by the NLRP3 inflammasome. Her lab identified a TRIF dependent pathway that licenses NLRP3 inflammasome activation through engagement of the caspase-11 protease. Finally, newer work in her lab has begun to examine the impact of long non-coding RNA species which are induced during host-pathogen interactions and which in turn act to coordinate transcriptional responses in innate immunity.