Eva-Lena Stange
@eva-stange.bsky.social
PhD Candidate in Medical Microbiology at RWTH Aachen. She/her. Interested in neonatal liver immunology, host-microbe interactions and scRNASeq.
🎉 thread with short highlight recap here: bsky.app/profile/eva-...
Excited to share the preprint of my PhD work with @ntorow.bsky.social! We asked what T cells in the neonatal liver are doing. Main takeaways: they’re activated before weaning (unlike in most organs), show distinct microbial sensitivity, form microclusters, and have long-term consequences. 🧵⏬(1/10)
January 15, 2026 at 9:34 AM
🎉 thread with short highlight recap here: bsky.app/profile/eva-...
Taken together: The neonatal liver undergoes a developmentally hard-wired Treg wave facilitated by cDC1s needed to restrain activation and promote tolerance in conventional T cells that respond to both microbes and self in early life. (10/10)
Link: tinyurl.com/neoliver
Link: tinyurl.com/neoliver
January 15, 2026 at 9:12 AM
Taken together: The neonatal liver undergoes a developmentally hard-wired Treg wave facilitated by cDC1s needed to restrain activation and promote tolerance in conventional T cells that respond to both microbes and self in early life. (10/10)
Link: tinyurl.com/neoliver
Link: tinyurl.com/neoliver
Yet, early-life Treg depletion also comes at a cost for long-term liver homeostasis: male mice depleted neonatally showed increased weight gain and steatosis, plus an aberrant T cell response when challenged with a high-fat diet --> even 2 months after the neonatal depletion window. (9/10)
January 15, 2026 at 9:12 AM
Yet, early-life Treg depletion also comes at a cost for long-term liver homeostasis: male mice depleted neonatally showed increased weight gain and steatosis, plus an aberrant T cell response when challenged with a high-fat diet --> even 2 months after the neonatal depletion window. (9/10)
So what does this Treg-rich microenvironment do? We teamed up with the Billerbeck lab using the NrHV model (HCV-like hepacivirus). Neonates showed delayed viral clearance. Treg depletion accelerated clearance - strong evidence that this regulatory setpoint shapes antiviral control. (8/10)
January 15, 2026 at 9:12 AM
So what does this Treg-rich microenvironment do? We teamed up with the Billerbeck lab using the NrHV model (HCV-like hepacivirus). Neonates showed delayed viral clearance. Treg depletion accelerated clearance - strong evidence that this regulatory setpoint shapes antiviral control. (8/10)
To understand where this happens, I designed a liver-immune–centric Xenium panel. Spatial mapping revealed that cDC1 colocalize with T cells in microclusters and are required for Treg accumulation. We also saw high Cxcl10 expression within clusters (ideas on the driver/source welcome 👀). (7/10)
January 15, 2026 at 9:12 AM
To understand where this happens, I designed a liver-immune–centric Xenium panel. Spatial mapping revealed that cDC1 colocalize with T cells in microclusters and are required for Treg accumulation. We also saw high Cxcl10 expression within clusters (ideas on the driver/source welcome 👀). (7/10)
This points to Tregs acting as a developmentally encoded control mechanism in early life. Notably, T cell activation in neonatal liver reaches adult-like levels by ~P7, whereas gut T cell activation is delayed until weaning. (6/10)
January 15, 2026 at 9:12 AM
This points to Tregs acting as a developmentally encoded control mechanism in early life. Notably, T cell activation in neonatal liver reaches adult-like levels by ~P7, whereas gut T cell activation is delayed until weaning. (6/10)
We sanity-checked across multiple microbial exposure models - antibiotics, OMVs, reversible colonization (thanks to @ganalvonarburg.bsky.social[email protected] for technique sharing grant!) and [email protected]. No changes in Tregs, but increased Tconv activation (5/10)
January 15, 2026 at 9:12 AM
We sanity-checked across multiple microbial exposure models - antibiotics, OMVs, reversible colonization (thanks to @ganalvonarburg.bsky.social[email protected] for technique sharing grant!) and [email protected]. No changes in Tregs, but increased Tconv activation (5/10)
As neonatal Treg waves in lung/gut/skin have been proposed to be microbiota-dependent, we asked whether liver Tregs would drop in germ-free mice. Surprise: they did not. In contrast, liver Tconvs specifically responded to microbial stimuli: they were less activated in germ-free pups. (4/10)
January 15, 2026 at 9:12 AM
As neonatal Treg waves in lung/gut/skin have been proposed to be microbiota-dependent, we asked whether liver Tregs would drop in germ-free mice. Surprise: they did not. In contrast, liver Tconvs specifically responded to microbial stimuli: they were less activated in germ-free pups. (4/10)
We deeply profiled liver Tregs across time (scRNA-seq + flow cytometry) and found pronounced clonal expansion and activation shift in early postnatal days: from a naïve-like state to a highly suppressive effector program at the peak of the neonatal liver T cell wave. (3/10)
January 15, 2026 at 9:12 AM
We deeply profiled liver Tregs across time (scRNA-seq + flow cytometry) and found pronounced clonal expansion and activation shift in early postnatal days: from a naïve-like state to a highly suppressive effector program at the peak of the neonatal liver T cell wave. (3/10)
Like others, we observed a wave of Tregs in neonatal WT liver during week 1–2 after birth. But it wasn’t just Tregs: CD4⁺ Tconvs and CD8⁺ T cells were also highly enriched vs adult liver, and in situ we saw T cell microclusters containing Tregs in hepatic tissue. (2/10)
January 15, 2026 at 9:12 AM
Like others, we observed a wave of Tregs in neonatal WT liver during week 1–2 after birth. But it wasn’t just Tregs: CD4⁺ Tconvs and CD8⁺ T cells were also highly enriched vs adult liver, and in situ we saw T cell microclusters containing Tregs in hepatic tissue. (2/10)
