
Group Leader investigating mechanisms of innate immune activation @MonashBDI @MonashUni. Alumni of @UniMelb, @IIIBonn and @WEHI_research.
Melbourne, Victoria
Joined August 2018
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Very happy to see our latest work out in @emboreports
. Here we discover an unexpected role for IRF3 in STING-induced pro-inflammatory cytokine production: link.springer.com/article/10…
Enjoy!
NHMRC-funded researchers have developed 3D 'mini brains' that mimic the damage caused by multiple sclerosis (MS).
The breakthrough could help scientists better understand the condition and test potential treatments, offering new hope for the nearly 3 million people affected by MS.
Read more here: ow.ly/Uiij50ZTNjM
Dom De Nardo retweeted
Today, the Toll-like Receptors reveal a new mechanism of signal transduction: Receptor-Free Signal Transduction.
nature.com/articles/s41586-0…
🔊2 weeks to go! Free registration for ImmuMon 2026 closes Friday, 21st August 🔊 Stay tuned for the final programme! Register now 🔗 immumon.com
✨ Thank you to all of our sponsors for supporting ImmuMon 2026! ✨
Dom De Nardo retweeted
Our paper introduces membrane-impermeable caspase inhibitors that use GSDMD pores as their entry route.
Because these compounds can't cross an intact membrane, they enter only cells already forming GSDMD pores — before pore density exceeds the cell's repair capacity. This confers built-in specificity: the drug acts solely on pyroptotic cells, leaving apoptosis and healthy cells untouched, addressing the off-target toxicity that has limited earlier, cell-permeable caspase inhibitors.
The effect goes beyond arresting cell death. Cells already committed to pyroptosis reverse course and regain viability — a "Lazarus effect" that challenges the assumption that lytic cell death, once initiated, is irreversible.
In essence, these unexpected results could create new opportunities for precisely targeting inflammatory cell death while safeguarding healthy tissue.
Dom De Nardo retweeted
A new PAMP, a new innate immunity principle and a new preclinical application. I am so pleased to share our study on STING activation mechanisms in health and disease. Led by the fantastic Stephanie Ragland, follow the summary below for all we learned.
cell.com/immunity/fulltext/S…
Dom De Nardo retweeted
For >10 years, neutrophils have challenged a central assumption of inflammasome biology by secreting IL-1 without robust pyroptosis. Our new study shows that the local inflammatory milieu regulates neutrophil susceptibility to CASP1-dependent pyroptosis.
science.org/doi/10.1126/scia…
Dom De Nardo retweeted
Into nucleic acid immunity? 🌏 Join #NAIS2026 in Nara, Japan!
📅 Sept 16–18, 2026
🧬 Abstract deadline (extended): June 30
📝 Register by: July 31
Explore the latest in nucleic acid immunity & connect with global experts.
🔗 ifrec.osaka-u.ac.jp/nais26/i…
Our findings are supported by the recent exciting work from Søren Paludan's lab:
link.springer.com/article/10…
Dom De Nardo retweeted
Proud to share The E3-ome
A true collaborative effort to unify the human E3 ligase landscape, and create a shared foundation for the field
#Ubiquitin #E3Ligases @WEHI_research
cell.com/cell/fulltext/S0092…
Dom De Nardo retweeted
More than 60% of Australian medical researchers left active research roles between 2019 and 2024 because they could not make ends meet - while my costings from the Parliamentary Budget Office suggest the govt could more than double annual spending from the Medical Research Future Fund without any effect on its base level of funding.
The government has to act on this issue in this year's Budget - for our economy and for our health.
abc.net.au/news/2026-03-09/m…
Dom De Nardo retweeted
TRIFosomes found😀. Very proud of our team’s work to identify endogenous TRIFosome. Surprisingly whilst TRIFosomes activate NFKB, IFN signaling is from monomeric or dimeric TRIF. doi.org/10.1126/sciadv.aeb95…
Dom De Nardo retweeted
Important paper on human recessive TBK1 deficiency:
Human TBK1 deficiency: An expanded spectrum from autoinflammation to viral encephalitis rupress.org/jhi/article/2/2/…
Dom De Nardo retweeted
I am delighted to share our characterisation of natural antagonism of TLR7/8 in Nature Immunology. We propose a model where 2’O-Methyl RNA fragments keep TLR7/8 in check, preventing autoimmunity. > nature.com/articles/s41590-0…
Dom De Nardo retweeted
ASMR's pre-budget submission calls for two strategic investments:
1️⃣ Unlock the Medical Research Future Fund
2️⃣ 20% Boost to the Medical Research Endowment Account
Read our full submission and learn more about why this investment matters: lnkd.in/g6ggRnFs
Dom De Nardo retweeted
Today, leading medical researchers from across the nation are stepping into Parliament, joining my call for the government to release the funds being withheld from the Medical Research Future Fund.
We must fund medical research properly. With the Trump administration slashing healthcare spending in the United States, Australia has a unique opportunity to become a global leader in medical innovation and biotech.
With the stroke of a pen, the government could make it happen today.
theguardian.com/australia-ne…
Join me in supporting the Release the Medical Research Future Fund Campaign aamri.org.au/mrff/
Dom De Nardo retweeted
Very excited to share the latest work from our lab, which was published today in Nature!
nature.com/articles/s41586-0…
PhD graduate and now post-doc @SofiaDahlman, along with co-senior author Sam Forster from The Hudson, and lab members @SubDinesh
Dom De Nardo retweeted
In my opinion, this is the most important aging-related paper of the year! It identifies a critical protein that could eventually extend lifespan by many years. Not surprisingly, it involves DNA repair and regulation of the immune response. Below is a breakdown of the key points (via GPT-5):
What did they find and why important?
•Naked mole-rats live a very long time and rarely get cancer.
•A key reason is a tiny change in a cell sensor called cGAS. This sensor usually detects stray DNA inside cells and sounds an alarm to the immune system.
•In humans, cGAS can drift into the nucleus and get in the way of one of our best DNA repair tools (called homologous recombination). That means more un-fixed DNA damage over time.
•In naked mole-rats, four small amino acid changes in cGAS flip the script. Their version does not block repair. Instead, it helps the high-fidelity repair process work better.
Why is this big for aging?
•Aging is partly the story of accumulating DNA damage. Better repair means fewer mutations, less cellular dysfunction, and a slower march toward age-related diseases.
•If we can make human cGAS behave more like the mole-rat version, we might reduce the daily damage load, which could:
•Lower cancer risk
•Preserve tissue function longer
•Delay multiple age-related declines at once
How could this translate to people?
1.Drug design: Create small molecules that keep human cGAS from interfering with DNA repair inside the nucleus, while still letting it do its normal immune-sensing job in the cytosol.
2.Protein engineering or gene therapy: Introduce cGAS variants that mimic the mole-rat’s four changes in high-risk tissues, carefully and locally.
3.Biomarkers and screening: Use cGAS activity and DNA repair efficiency as readouts to find who might benefit and to measure whether a therapy is working.
4.Combination strategies: Pair cGAS-tuning with other repair boosters and senescence-reducers for a bigger effect.
Bottom line:
A few precise tweaks to one protein can shift the balance from ongoing damage toward cleaner, faster DNA repair. That is exactly the kind of leverage aging research needs: change a small control knob, get system-wide benefits. The naked mole-rat just showed us one such knob.
Paper link in the thread.
Dom De Nardo retweeted
Glad that our paper is officially out @CellCellPress. BRD4 condensate functions as a pH sensor to tune inflammatory response in macrophage. cell.com/cell/fulltext/S0092…
earlier post: xitter.cf/XuZhouLab/status/19459…
and could-have-been cover by my student&artist Cathleen Krabak @harvardmed
Beyond excited to share our #NewPaper in @CellCellPress! Inflamed environments acidify intracellular pH. BRD4 senses this via transcriptional condensates, tuning #macrophage responses to match demand and consequences of inflammation. #inflammation #pH authors.elsevier.com/sd/arti…


















