Feels timely to repost my commentary and call for action > Tech convergence and the unpredictable future of biothreats
nationaldefensemagazine.org/…
New approach methodologies (#NAMs) + computation may give us a new way to untangle one of the most devastating immune complications of transplantation.
That is the premise behind our newly funded NIH R01 focused on pediatric acute graft-versus-host disease (#GVHD). For children undergoing bone marrow transplantation, the transplant itself often comes after an already difficult journey with serious disease. GVHD can add another major complication, when the donor immune system meant to help save a child’s life instead begins attacking their tissues.
Our goal is to build patient-specific digital twins that connect what is happening in an individual child with experimentally tractable human models and computational prediction.
By combining patient samples, human tissue and microphysiological systems, immunogenetics, and systems-level modeling, we aim to understand why GVHD develops so differently from patient to patient—and ultimately create tools that can support more precise, individualized treatment.
Just as important is how this project came together. At Johns Hopkins All Children's Hospital, the close connection between basic science and clinical medicine makes it possible to build projects around questions that emerge directly from patient care. Our work at the Institute for Fundamental Biomedical Research joins forces with the clinical expertise of Minelys Alicea Marrero and Michael Wilsey, Scott Krummey and the Immunogenetics Laboratory at The Johns Hopkins University School of Medicine, and Duglas Brubaker’s systems biology and computational modeling program at Case Western Reserve University.
The larger idea is simple > use human biology to understand human disease, and computation to turn those observations into prediction.
Thanks to Institute of Allergy and Infectious Diseases (#NIAID) we get to build it.
#humanbiomimetics
I had the immense pleasure of spending a morning with high school students at 2. Gimnazija Maribor discussing the future of medicine, and what a “Human 2.0” might look like.
We talked about stem cells, organoids, regenerative medicine, organ-on-chip systems, AI/automation driven labs, and the many ways cells are changing how we understand and treat disease.
But what I hope they took away is something broader.
Despite the uncertainty of the current moment, and despite the understandable anxiety created by constant narratives about AI, replacement, and disruption, the reality is much more open, and much more hopeful.
The biggest discoveries are still ahead of us.
The hardest diseases still need to be cured.
The most important tools still need to be built.
And it will take a village: biologists, physicians, chemists, engineers, material scientists, computer scientists, ethicists, builders, communicators, and many others.
If young people can tune out some of the noise and let curiosity take over, there is an enormous amount of meaningful work waiting for them.
Despite the uncertainty of the current moment, and despite the understandable anxiety created by constant narratives about AI, replacement, and disruption, the reality is much more open, and much more hopeful.
The biggest discoveries are still ahead of us.
The hardest diseases still need to be cured.
The most important tools still need to be built.
And it will take a village: biologists, physicians, chemists, engineers, material scientists, computer scientists, ethicists, builders, communicators, and many others.
If young people can tune out some of the noise and let curiosity take over, there is an enormous amount of meaningful work waiting for them.
Martin Trapecar retweeted
New commentary Immune-competent new approach methodologies for a hybrid future (w/ animal models) just out @NatImmunol! Congrats to co-1st authors @VanceSoares & @victorquiroz68! And co-corresponding authors @MTrapecar & @deokkim1!
nature.com/articles/s41590-0…
@JHUBME @TTECJHU
Martin Trapecar retweeted
Academia feels increasingly like playing Monkey Island, if you miss something as absurd as picking up a rubber chicken with a pulley in the first scene, you only realize much later that you’re stuck and can’t pass to the next stage.
I was interviewed today by @ScienceMagazine about the funding crisis following the ERC announcement. I argued that when a grant rejection can hinge on something small, and you then have to wait years to resubmit, the cost becomes so high that instead of suggesting “high-risk high-gain” plans scientists will prepare more cautious, less ambitious proposals. It turns into a perverse game of simplifying your ideas and trying (unsuccessfully) to predict what an overstretched reviewer pool will find easiest to digest.
"Abrupt change to European funder’s rules leaves researchers shut out | Science | AAAS" science.org/content/article/…
🚀 New paper out (Open Access): a same-donor, cross-tissue scRNA-seq + TCR-seq map of T cells across the human **gut–liver–blood axis**.
The gut–liver axis is arguably the body’s most immunologically active interface, where constant exposure to dietary and microbial antigens meets the liver’s high-volume immune filtration. Yet we still poorly understand how individual T-cell clones are connected across multiple organs within the same person via circulation and tissue seeding. Strikingly, even within a single organ the colon’s IEL and lamina propria T-cell compartments behave like distinct ecosystems, showing huge diversity and surprisingly little clonal overlap despite being separated by only microns.
Key takeaways:
📈 Across tissues, highly expanded clones share a core “clonal success” transcriptional signature
🧩 Niche signaling points to **liver-derived ligands shaping colon TRM states** (via integrin-linked axes)
🧭 Tissue-resident programs diverge strongly across sites (colon vs liver), with LP TRMs enriched for interferon-stimulated programs
🔀 **IEL vs lamina propria** clonotype overlap is *modest* → limited exchange between these compartments
🔥 In liver, **MAIT cells dominate the most expanded clonotypes**
If you care about tissue-resident immunity, MAIT biology, or how immune circuits adapt across connected organs, I’d love to hear what resonates (and what you’d want to see next).
👇 Paper link in the comments.
#CellReports #SingleCell #Immunology #TCells #TissueResident #Gut #Liver #humanbiomimetics #JHACH #JHU
Would you like to break open a new frontier in fighting pediatric brain cancers? Join us > nature.com/naturecareers/job…
Immunologist’s “immunocompetent”: innate sensors fire, APC relay, T-cells boom, B-cells class-switch, antibodies refine, memory locks in. Bioengineer: sprinkled monocytes on a chip. #NotTheSameThing
New #bioRxiv preprint with @_DougBru ! We explored T cell diversity & clonal dynamics across the human gut-liver-blood axis using single-cell RNA & TCR sequencing of matched samples. 1/3 biorxiv.org/content/10.1101/… #immunology #Tcells #scRNAseq
This work highlights the importance of studying human immunity in situ & has implications for understanding tissue-specific diseases. #gutliveraxis #tissueimmunity #humanimmunology
Tech convergance and unpredictable future of biothreats
nationaldefensemagazine.org/…
#defense #CBRN #bioweapons
When one’s cover letter says:”I am particularly drawn to this opportunity [specific aspects of the lab ,e.g., its focus in chromatin dynamics or translational applications]. I am confident that my technical expertise aligns well with the goals of your team.”
We are hiring
nature.com/naturecareers/job…
Martin Trapecar retweeted
Our preprint: Systematic Analysis of Human Colorectal Cancer scRNA-seq Revealed Limited Pro-tumoral IL-17 Production Potential in Gamma Delta T Cells biorxiv.org/content/10.1101/…
@forum_gd @_DougBrubaker @MTrapecar
#Immunology #gdTcells #Cancer #colorectalcancer






