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Dominic De Nardo
Researcher at Monash University, Clayton campus
Publications - 56
Citations - 6684
Dominic De Nardo is an academic researcher from Monash University, Clayton campus. The author has contributed to research in topics: Innate immune system & Inflammasome. The author has an hindex of 28, co-authored 46 publications receiving 4901 citations. Previous affiliations of Dominic De Nardo include Cooperative Research Centre & Monash University.
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Journal ArticleDOI
Transcriptome-Based Network Analysis Reveals a Spectrum Model of Human Macrophage Activation
Jia Xue,Susanne Schmidt,Jil Sander,Astrid M. Draffehn,Wolfgang Krebs,Inga Quester,Dominic De Nardo,Trupti D. Gohel,Martina Emde,Lisa Schmidleithner,Hariharasudan Ganesan,Andrea Niño-Castro,Michael R. Mallmann,Larisa I. Labzin,Heidi Theis,Michael Kraut,Marc Beyer,Eicke Latz,Eicke Latz,Tom C. Freeman,Thomas Ulas,Joachim L. Schultze +21 more
TL;DR: By integrating murine data from the ImmGen project, this work proposes a refined, activation-independent core signature for human and murine macrophages that serves as a framework for future research into regulation of macrophage activation in health and disease.
Journal ArticleDOI
The adaptor ASC has extracellular and 'prionoid' activities that propagate inflammation
Bernardo S. Franklin,Lukas Bossaller,Dominic De Nardo,Jacqueline M Ratter,Andrea Stutz,Gudrun Engels,Christoph Brenker,Mark Nordhoff,Sandra R Mirandola,Ashraf Al-Amoudi,Matthew Mangan,Sebastian Zimmer,Brian G. Monks,Martin Fricke,Reinhold E. Schmidt,Terje Espevik,Bernadette Jones,Andrew G. Jarnicki,Philip M. Hansbro,Patricia Busto,Ann Marshak-Rothstein,Simone Hornemann,Adriano Aguzzi,Wolfgang Kastenmüller,Eicke Latz +24 more
TL;DR: It is found that after pyroptosis, ASC specks accumulated in the extracellular space, where they promoted further maturation of IL-1β, and a previously unknown form of cell-to-cell communication is revealed.
Journal ArticleDOI
NLRP3 inflammasomes link inflammation and metabolic disease.
TL;DR: New developments in the activation of the NLRP3 inflammasome, an interleukin-1β family cytokine-activating protein complex, in a variety of metabolic diseases including obesity, atherosclerosis and type 2 diabetes are reviewed.
Journal ArticleDOI
TDP-43 Triggers Mitochondrial DNA Release via mPTP to Activate cGAS/STING in ALS
Chien-Hsiung Yu,Chien-Hsiung Yu,Sophia Davidson,Sophia Davidson,Cassandra R. Harapas,Cassandra R. Harapas,James B. Hilton,James B. Hilton,Michael J. Mlodzianoski,Michael J. Mlodzianoski,Pawat Laohamonthonkul,Pawat Laohamonthonkul,Cynthia Louis,Cynthia Louis,Ronnie Ren Jie Low,Ronnie Ren Jie Low,Jonas Moecking,Jonas Moecking,Jonas Moecking,Dominic De Nardo,Dominic De Nardo,Dominic De Nardo,Katherine R. Balka,Katherine R. Balka,Katherine R. Balka,Dale J. Calleja,Dale J. Calleja,Fiona Moghaddas,Fiona Moghaddas,Fiona Moghaddas,Erya Ni,Erya Ni,Catriona McLean,Andre L. Samson,Andre L. Samson,Shiraz Tyebji,Shiraz Tyebji,Christopher J. Tonkin,Christopher J. Tonkin,Christopher R. Bye,Bradley J. Turner,Genevieve Pepin,Genevieve Pepin,Michael P. Gantier,Michael P. Gantier,Kelly L. Rogers,Kelly L. Rogers,Kate McArthur,Peter J. Crouch,Peter J. Crouch,Seth L. Masters,Seth L. Masters +51 more
TL;DR: The results identify mtDNA release and cGAS/STING activation as critical determinants of TDP-43-associated pathology and demonstrate the potential for targeting this pathway in ALS.
Journal ArticleDOI
High-density lipoprotein mediates anti-inflammatory reprogramming of macrophages via the transcriptional regulator ATF3
Dominic De Nardo,Larisa I. Labzin,Hajime Kono,Reiko Seki,Susanne Schmidt,Marc Beyer,Dakang Xu,Sebastian Zimmer,Catharina Lahrmann,Frank A. Schildberg,Johanna Vogelhuber,Michael Kraut,Thomas Ulas,Anja Kerksiek,Wolfgang Krebs,Niklas Bode,Alena Grebe,Michael L. Fitzgerald,Nicholas J. Hernandez,Bryan R.G. Williams,Percy A. Knolle,Manfred Kneilling,Martin Röcken,Dieter Lütjohann,Samuel D. Wright,Joachim L. Schultze,Eicke Latz +26 more
TL;DR: The transcriptional regulator ATF3 is identified, as an HDL-inducible target gene in macrophages that downregulates the expression of Toll-like receptor (TLR)-induced proinflammatory cytokines and may explain the broad anti-inflammatory and metabolic actions of HDL.