Mass Lab

#Microglia and CD8⁺ T cell activation precede neuronal loss in a murine model of spastic paraplegia 15. From Frolov, @haohuang0086.bsky.social, Stumm, @masslab.bsky.social, Beyer et al.: rupress.org/jem/article/...

📘 In our #Neuroscience collection: rupress.org/jem/collecti...
#SfN25

Characterization of the mammalian prodefinitive angio-hematopoietic lineage The identification of mammalian prodefinitive angio-hematopoietic progenitors clarifies early hematopoiesis and macrophage development.

Happy to have contributed to this beautiful story on #macrophage #development in mice and in #iPSC derived cells.
www.science.org/doi/10.1126/...
Big congrats to first author Tomi Lazarov for this massive work!!!!👏

Interested in #macrophages? Don't forget the check out this Seminar Series 👇

The Vienna BioCenter PhD Program application deadline is approaching: October 10!

Join one of Europe’s premier life science campuses, home to cutting-edge research across all areas of biology.
Apply and start your scientific journey in Vienna!

training.vbc.ac.at/phd-program/

#PhD #LifeSciences

🔔PhD position open. Interested in building competencies in computational biology in spatial transcriptomics? Malte Luecken's lab and I have an open PhD position, part of the Munich School of Data Science.
Application deadline: Sept 26
Link: www.mu-ds.de

Had the wonderful opportunity to present our data on the effect of microplastics on macrophages at #EMDS2025 ! Such a beautiful venue 🤩 @masslab.bsky.social

Flyer advertising the BonnBrain Conference 2026, "From Genes to Circuits and Behavior".

Application is open! Come join us and our fantastic line-up of speakers next year in March in Bonn!

BBS8-dependent ciliary Hedgehog signaling governs cell fate in the white adipose tissue | The EMBO Journal imageimageDisruption of ciliogenesis in Bardet-Biedl syndrome (BBS) leads to obesity and disrupted adipogenesis. This study reveals that ciliary dysfunction in a mouse model of BBS induces a a cell fa...

🚨 New in The EMBO Journal!
Loss of BBS8 disrupts ciliary Hedgehog signaling, switching adipocyte precursors into fibrogenic cells—remodeling adipose tissue before obesity begins.
🔬 #BBS #cilia @for5547.bsky.social @sfb1454.bsky.social @batenergy.bsky.social
📄 www.embopress.org/doi/full/10....

Description Please note that job descriptions are not exhaustive, and you may be asked to take on additional duties that align with the key responsibilities ment...

Come be my colleague! We have three open positions at the Assistant/Associate Professor level for candidates in all areas of the biological sciences.

www.imperial.ac.uk/jobs/search-...

#WomenInSTEM becoming independent: People should feel free to be themselves and do great science. We asked ten women researchers about their science and the process of setting up a lab as an independent researcher: rupress.org/jem/article/...

Setting the table for immune tolerance Interaction between breast milk antibodies and gut microbes shape immune responses during weaning

Out today! www.science.org/doi/10.1126/... From @kknoop.bsky.social & myself on early life immune development & the beautiful publication from Megan Koch & M Shenoy www.science.org/doi/10.1126/... Take home message: timing of early life exposures, milk IgG here, is critical for immune development.

COVER This illustration depicts the changes in the immune system throughout an individual’s life span, from infancy to childhood, adulthood, and older age. The infant silhouette contains DNA, and the figures are enveloped by the nuclear and plasma membranes. These components reference the evolution of immunity over millennia, as viruses integrated into the genome and as life progressed from single-celled to multicellular organisms. See the special section beginning on page 586. Illustration: Rioka Hayama

This week's @science.org #IMMUNOLOGY-themed SPECIAL ISSUE features Reviews by {Kassiotis & Stoye}, {Nahrendorf, Ginhoux, & Swirski}, {Sharma, Gibbons, & Saphire}, & {@jessmetcalf.bsky.social, @grahammunology.bsky.social, Yates, & Cummings} + an absolutely wild & wonderful cover!

scim.ag/3UqRrA6

Our recent overview of human stem cell models for studying neuropsychiatric disorders (including their limitations and future directions) is now openly available @annualreviews.bsky.social of Neuroscience

With the great @rebeccalevymdphd.bsky.social

🧠 New book chapter out!

We review the developmental origin and functional diversity of #microglia - key players at the crossroads of #immunity and #neurodevelopment.

🔹 Ontogeny & specialization
🔹 Transcriptional & metabolic shifts
🔹 Roles in disease & repair
👉 authors.elsevier.com/a/1lKxcErwXf...

4/Together, these studies highlight the evolutionarily #conserved and multi-organ impact of maternal diet on offspring health and disease susceptibility.

Huge thanks to Seyhmus Bayar and our collaborators for their fantastic work!
@for5775.bsky.social

Kupffer cell programming by maternal obesity triggers fatty liver disease - Nature In a mouse model, maternal obesity during pregnancy can lead to fatty liver disease in the offspring, driven by aberrant developmental programming of Kuppfer cells.

3/ This work builds on our previous findings published in @nature.com (Huang et al., 2025), where we showed that yolk sac-derived Kupffer cells mediate fetal liver programming in obese pregnancies, driving fatty liver disease in adulthood (www.nature.com/articles/s41...)

2/In this study, we uncover how maternal diet in flies(corresponding to maternal obesity in mammals) disrupts #neuronal integrity and #immune function in offspring. We identify axon #degeneration and shortened #lifespan, linking maternal overnutrition to long-term health consequences.

Developmental programming by maternal obesity alters offspring lifespan and immune responses in a diet- and sex-specific manner Maternal obesity is a growing health concern that predisposes offspring to metabolic dysfunction, immune system alterations, and neurodegenerative dis…

1/ 💡We are excited to share our latest paper, continuing our exploration of how maternal obesity programs offspring health via #macrophages - this time using #Drosophila as a model: shorturl.at/28tFo

#MaternalObesity #Drosophila #Neurodegeneration #DOHaD #FlyResearch #MacrophageBiology

1/ 🚨 Hot off the press in Nature Immunology: CD4⁺ T cells can license Kupffer cells to rescue dysfunctional CD8⁺ T cells in the liver. Hepatitis B virus (HBV) infection is just the proving ground—this is a paradigm shift in tissue immunity. www.nature.com/articles/s41... 🧵(1/11)

Research Associate in Mucosal Immunology :Manchester

The fantastic Menon Lab (@madhvimenon.bsky.social) in the @lydiabeckeriii.bsky.social in Manchester are hiring!!
🚨DO NOT MISS YOUR CHANCE TO APPLY!🚨

www.jobs.manchester.ac.uk/Job/JobDetai...

Postdoc seeking to unravel how lung-infiltrating #Bcells contribute to chronic lung disease #immunosky

🧪 One month until the application deadline. Get in touch if you are interested ⬇️
#immunosky #cardiosky #academicsky #ecr #studyintheuk

Led by @haohuang0086.bsky.social and Nora R. Balzer
📍 Developmental Biology of the Immune System, LIMES Institute
#DOHaD #macrophages #FattyLiverDisease

12/
Big thanks to all collaborators across @sfb1454.bsky.social @unibonn.bsky.social @limes-bonn.bsky.social @dzne.science

11/
🧠 This aligns with the concept of DOHaD (Developmental Origins of Health and Disease) — and adds tissue-resident macrophages to the list of intergenerational regulators.

10/
🚨 Implication:
We identify a therapeutic window during gestation to target fetal KC programming — potentially preventing metabolic liver disease in later life.

9/
This work shifts the paradigm:
🔁 FLD is not just a postnatal diet effect
🧬 It can originate from developmental #macrophage programming — long before birth

8/
Live-imaging of hepatocytes exposed to ApoE confirmed:
→ ApoE and ApoA1 alone was sufficient to cause lipid droplet accumulation

7/
Multi-omics profiling (bulk & single-nucleus RNA-seq + ATAC-seq + proteomics) revealed:
✅ Apolipoproteins ApoE and ApoA1 are upregulated in reprogrammed KCs
✅ They act via paracrine signaling to induce steatosis in hepatocytes

6/
Using a double fate-mapping model, we confirm that these disease-driving KCs remain yolk sac–derived — not replaced by monocyte-derived macrophages, as seen in diet-induced FLD.

5/
💥 Strikingly, depleting KCs at birth and replacing them with monocytes from lean animals rescued the FLD phenotype — directly implicating programmed KCs as causal agents.