Dominic De Nardo

Dominic De Nardo

Institute of Innate Immunity
University Hospital
University of Bonn

Dr Dominic De Nardo received his PhD in 2009 from the University of Melbourne, Australia, where he developed a keen interest in macrophages and the innate immune system while working on mechanisms of Toll-like receptor activation. In 2010 he accepted a postdoctoral position with Prof Eicke Latz at the Institute of Innate Immunity in Bonn, Germany, where his research focuses on understanding the mechanisms controlling activation and regulation of innate immune receptors and signaling pathways, and their roles in inflammation during health and disease. During his postdoc Dominic identified the molecular mechanism underlying the ability of HDL to reduce inflammation, co-authored several studies published in journals such as Nature Immunology and Immunity, was invited to edit the innate immunity section of Current Opinion in Immunology and secured funding to lead a junior group. In late 2014 Dominic will return to his homeland to continue his research in the laboratory of Dr Seth Masters within the Inflammation Division at the Walter and Eliza Hall Institute of Medical Research in Melbourne.

Stacy Horner

Stacy Horner

Molecular Genetics and Microbiology
Duke University Medical Center
Durham, NC

Dr. Stacy Horner is currently an Assistant Professor in the Molecular Genetics & Microbiology and Medicine departments at Duke University Medical Center. She received her Ph.D. in 2007 from Yale University under the mentorship of Dr. Daniel DiMaio. Her postdoctoral fellowship, which was supported by the Irvington Institute Fellowship Program of the Cancer Research Institute, was with Dr. Michael Gale Jr. at the University of Washington. Her postdoctoral research focused on understanding innate immune regulation by hepatitis C virus (HCV), a global human pathogen. During this time, she identified the mitochondrial-associated ER membrane (MAM; a subdomain of the ER located adjacent to mitochondria) as a membrane platform that organizes innate immune signaling to RNA viruses and serves as the intracellular site of immune regulation by HCV. Her current research focuses on understanding the organization and regulation of antiviral innate immunity and how RNA viruses, including HCV, evade innate immunity. Research in her laboratory uses an interdisciplinary approach, combining techniques from cell biology, virology, biochemistry, and systems biology to reveal the viral and host strategies that coordinate and regulate innate immunity to RNA viruses, with the ultimate goal of developing new immunomodulatory strategies for virus treatment and prevention.

Maria Liaskos

Maria Liaskos

Centre for Innate Immunity and Infectious Diseases
MIMR-PHI Institute of Medical Research
Melbourne, Australia

Dr Maria Kaparakis-Liaskos obtained her Ph.D from the Department of Microbiology and Immunology at the University of Melbourne in 2005, under the supervision of Professor Richard Strugnell. Since graduating, Dr Liaskos research interests have focused on understanding the mechanisms underlying the induction of inflammation and pathology in response to bacterial infection, and in particular, to the gastric pathogen Helicobacter pylori.

Dr Liaskos undertook her post-doctoral studies in the laboratory of Associate Professor Richard Ferrero at Monash University, where she examined innate immune responses to Helicobacter pylori. During this time, she and her colleagues identified bacterial outer membrane vesicles as a novel mechanism whereby all Gram negative bacteria, irrespective of their mode of infection, could be detected by the intracellular pathogen recognition receptor, NOD1.

In 2009, Dr Liaskos joined the Centre of Innate Immunity and Infectious Diseases, at Monash Institute of Medical research, now named the MIMR-PHI Institute of Medical Research. Her current research focuses on understanding the role of NOD1 in responding to bacterial infections and in the development of pro-inflammatory cytokine responses. Her recent research has identified the intracellular location of NOD1, as well as the mechanisms whereby NOD1 detects Gram negative bacterial peptidoglycan, resulting in the generation of autophagy and the production of pro-inflammatory cytokines by the host. These recent findings elucidate the cellular processes underlying NOD1-driven pathology and have the potential to advance the design and development of therapeutics against NOD-Like Receptor (NLR) driven disease states.

Seth Masters

Seth Masters

Inflammation Division
The Walter and Eliza Hall Institute

Victoria, Australia

Dr Masters completed his PhD at the Walter and Eliza Hall Institute (WEHI), which resulted in the first structure of the SPRY/B30.2 domain. In 2006 Dr Masters started a postdoc with Dan Kastner at the NIH who previously discovered mutations in the SPRY/B30.2 domain of the protein Pyrin, which cause familial Mediterranean fever. During this postdoc he was part of a team that discovered a new inflammatory disease caused by mutations affecting the IL-1 receptor antagonist (IL-1Ra). Starting in 2009, Dr Masters completed a second postdoc at Trinity College Dublin where he continued to work on IL-1. Research here showed that soluble oligomers of IAPP, which are increased in type 2 diabetes, trigger the NLRP3 inflammasome to process IL-1b, which impairs the function of insulin producing beta cells. Dr Masters has now started his own laboratory in the newly formed Inflammation Division at WEHI, and has published on miRNA regulation of the NLRP3 inflammasome and the first mouse models of NLRP1 inflammasome modulation. Seth has been on the ICIS Awards Committee since 2017.

Kate Schroder

Kate Schroder

Institute for Molecular Bioscience
The University of Queensland

Brisbane, Australia

Kate Schroder’s research focuses on the interactions between host and pathogen during the initial stages of infection and the development of inflammation. She received her PhD in 2005 for studies investigating mechanisms of cross-talk between innate immune signalling pathways (interferon-gamma and Toll-like receptors), in the laboratory of David Hume. Her subsequent postdoctoral position with David Hume and Matthew Sweet investigated the transcriptional programs triggered by macrophage differentiation and Toll-like receptor ligation. A key focus of her postdoctoral studies was to define species differences in the TLR4-dependent responses of human versus mouse macrophages. During her NHMRC CJ Martin Fellow in Jurg Tschopp’s group in Switzerland, Kate gained expertise in Nod-like receptor function and inflammasome signalling. She returned to Australia in 2011, and now heads the Inflammasome Laboratory of the Institute for Molecular Bioscience, University of Queensland, as an ARC Future Fellow. Her current research interests include mechanisms of signal integration between inflammasomes and other innate immune pathways (e.g. TLRs), the molecular mechanisms governing inflammasome and caspase activation, the evolutionary biology of inflammasomes, and the cellular mediators of inflammasome-dependent inflammation. The Inflammasome Laboratory 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.