Kate Schroder

Background

About Kate Schroder

The innate immune system is the body’s first line of defence against microbial attack. The innate immune system recognises such situations of cellular ‘danger’ through receptors such as the Nod-like Receptors (NLRs), which recognise microbial structures and launch antimicrobial defence mechanisms. Many NLRs do so by forming molecular complexes called inflammasomes in response to cellular infection with pathogenic bacteria, viruses and fungi. Inflammasomes provide a molecular platform for cluster-dependent activation of the protease, caspase-1, and thereby elicit a proteolytic signalling pathway that triggers the processing and secretion of proinflammatory mediators, and drives inflammatory cell death. These pathways culminate in immune system activation (inflammation), the induction of antimicrobial defence mechanisms, and microbial elimination. Inflammasomes can also be triggered by non-microbial structures (e.g. host molecules indicating cell stress or injury) and can thereby drive unhealthy inflammation in human disease. Genetic mutations in 8 NLR family members are associated with human heritable inflammatory disorders, and recent studies have identified an unexpected role for inflammasome-dependent cytokines in driving the inflammatory component of numerous chronic diseases (e.g. gout, diabetes, Alzheimer's disease). Kate Schroder’s research focuses on the mechanisms by which inflammasomes drive inflammation. Her research interests include signal integration between inflammasomes and other innate immune pathways (e.g. TLRs), the molecular mechanisms governing inflammasome activity, the evolutionary biology of inflammasomes, and the cellular mediators of inflammasome-dependent inflammation. The Inflammasome Laboratory at IMB integrates molecular and cell biology approaches with in vivo studies to gain a holistic understanding of inflammasome function during infection, and inflammasome dysfunction in human inflammatory disease.