Our laboratory studies the molecules that govern the often-connected processes of cell death and inflammation. These processes normally protect against microbial infection, and allow tissue repair. Loss of control of cell death and inflammation underpins diseases such as sepsis, rheumatoid arthritis and cancer.
Our goal is to understand how cell death and inflammation are controlled, as a basis for new treatments for these diseases.
Our research focuses on the receptors and molecular signalling networks that cause cell death and inflammation. A particular interest is understanding how the potent pro-inflammatory protein, interleukin-1 (IL-1), is activated and promotes pathology in inflammatory diseases. Understanding how IL-1 activity is controlled will allow the targeted design of next-generation anti-inflammatory therapeutics.
We are also investigating the role of pattern recognition receptors (PRRs) in inflammation. PRRs detect pathogenic microbial organisms and trigger innate immune responses. However, changes in PRRactivity are responsible for inflammatory diseases, including atherosclerosis, diabetes and arthritis.
We study PRRs called inflammasomes that promote pro-inflammatory cytokine activation and cause pyroptosis, a programmed form of inflammatory cell death. We are investigating how inflammasomes are regulated in innate immune cells and its relevance to health.
Our recent research revealed molecular links between apoptotic and necroptotic cell death and inflammatory cytokine production, including inflammasome activity. We are continuing to decipher exactly how cell death and inflammation are inextricably linked at the molecular level.