Research Interests

Kate Fitzgerald's laboratory is interested in understanding how the innate immune system distinguishes friend from foe to drive protective inflammatory responses. Her early work on Toll-like receptor signaling established some of the founding principles underlying the induction of pathogen-specific responses. Similarly, her discovery of TANK-Binding Kinase-1, the kinase that phosphorylates and activates interferon regulatory factors, paved the way for a greater understanding of interferon gene regulation and induction of anti-viral immunity. Her research to characterize inflammasome activation led to the discovery of Absent in Melanoma-2 as a new receptor. Her group has also defined the central role of nucleic acids as triggers of anti-microbial immunity and described new sensors and regulators of these pathways. She has also explored how the inappropriate activation of nucleic acid-sensing pathways and inflammasome pathways underlies the pathogenesis of inflammatory and autoimmune diseases. More recently, she has conducted groundbreaking work on the role of long non-coding RNAs in the inflammatory response. At their core, these studies explore fundamental aspects of host defense and inflammatory diseases. The long-term goal of her work is to determine how the inappropriate activation of innate immunity underlies the pathogenesis of infectious, inflammatory, and autoimmune diseases in humans.

Membership Type


Election Year


Primary Section

Section 43: Immunology and Inflammation

Secondary Section

Section 44: Microbial Biology