Asma Farhat

Asma Farhat Asma Farhat on Simons Foundation

Congrats to superstar @asmafarhat.bsky.social for being selected as a Simons Postdoctoral fellow to study how inflammation impacts sensory development and function in the Naik lab and Allen Discovery Center. @simonsfoundation.org @sinaiimmuno.bsky.social
www.simonsfoundation.org/people/asma-...

Congrats to @asmafarhat.bsky.social from the group of former #CeMM PI Sylvia Knapp (@knapplab.bsky.social), on successfully defending her PhD thesis entitled "From Bone to Breath: How hematopoietic aging shapes macrophage fate, function & lung fibrosis." Well done!! 🎓 👏 🎉 #phdlife #phdhat

Endothelial-driven TGFβ signaling supports lung interstitial macrophage development from monocytes Endothelial Tgfβ1 shapes the development and functional identity of lung interstitial macrophages.

#WeekendRead! #EveryCellIsAnImmuneCell! Peng Bai Marichal &co show @ Science Immunology that endothelial cells produce TGFb to differentiate monocytes into #lung interstitial macrophages preventing aging & fibrosis
www.science.org/doi/10.1126/...

Congrats to Sylvia Knapp and team on their new Science Immunology paper! They show how aged bone marrow drives lung fibrosis by sustaining profibrotic macrophages. Reduced T-reg IL-10 worsens healing, revealing key immune-aging links.

www.science.org/doi/10.1126/...

#Immunology #LungFibrosis

Staphylococcus aureus skin infection induces eosinophil innate immune memory to exacerbate allergen-induced airway inflammation @sciimmunology.bsky.social
www.science.org/doi/10.1126/...

Huge congratulations to @mariemradhouani.bsky.social who spearheaded this brilliant and seminal study out now in Science Immunology @science.org !!

science.org/doi/10.1126/sciimmunol.adp6231

Lucky to have been a part of this team from @starkllab.bsky.social

Read more on Mariem's thread below!

An aging bone marrow exacerbates lung fibrosis by fueling profibrotic macrophage persistence Hematopoietic aging drives lung fibrosis and profibrotic macrophage influx, stalling their maturation via reduced Treg-derived IL-10.

Using a fibrosis model in young vs aged mice, Farhat and Knapp show that an aged bone marrow autonomously produced more profibrotic Mo-AMs, had a reduced availability of Tregs-derived IL-10 causing exacerbated lung fibrosis. [4/n]

www.science.org/doi/10.1126/...

Lung Macrophages — payal yokota

Here, we go. Starting 2025 best lung papers. Will add as I go along and also updated on the blog.

payalyokota.com/lung-macroph...

Thank you @chrysante-ili.bsky.social!

Thank you @payalyokota.bsky.social!!

Very cool (and surreal!) seeing my paper featured on the Science homepage www.science.org !! #ScienceImmunology
science.org/doi/10.1126/sciimmunol.adk5041

Huge thanks to our collaborators and wonderful co-authors who made this possible! @mariemradhouani.bsky.social @floriandeckert.bsky.social @SophieZahalka @Lisabeth Pimenov @Alina and all others on and off Bluesky!!
@MedUni Vienna @CeMM #ScienceImmunology

10/ Our study highlights the impact of an aging bone marrow on the lung and defines a Treg–IL-10–macrophage axis that becomes dysfunctional with age. It offers a potential immune axis to reduce fibrotic severity and reframes how we understand age-related tissue dysfunction.

9/ Conversely, transplanting young bone marrow into aged mice reduced disease severity and profibrotic macrophage numbers - showing that the age of the bone marrow shaped fibrotic outcome.

8/ Blocking IL-10 or depleting Tregs in young mice reproduced the aged bone marrow phenotype. Mo-AMs failed to mature and fibrosis worsened.

7/ This failure was linked to reduced IL-10 in the lung, a key anti-inflammatory cytokine.
The reason: fewer IL-10–producing regulatory T cells (Tregs) in the lungs of mice with aged bone marrow.

6/ We found that not only were Mo-AM numbers higher, but these aged Mo-AMs failed to transition into a tissue-resident, homeostatic state. They remained persistently inflammatory and profibrotic over time.

5/ Aged bone marrow caused increased recruitment of monocytes and accumulation of monocyte-derived alveolar macrophages (Mo-AMs)—key immune players in fibrosis.

4/ Transplanting aged bone marrow cells into young mice led to more severe lung fibrosis after injury—despite the lung tissue being young.
This points to the aging immune system as a key driver of fibrotic progression.

3/ We asked: Can hematopoietic aging drive lung fibrosis? To test this, we used a bone marrow transplant model to decouple immune and lung tissue aging.

2/ Lung fibrosis is a devastating, end-stage disease with limited treatment options. Aging is the strongest risk factor, but how immune aging contributes remains poorly understood

An aging bone marrow exacerbates lung fibrosis by fueling profibrotic macrophage persistence Hematopoietic aging drives lung fibrosis and profibrotic macrophage influx, stalling their maturation via reduced Treg-derived IL-10.

1/ Excited to share my first-ever first-author paper out now in Science Immunology! from @knapplab.bsky.social and co-supervised by @miershawig.bsky.social
We show that hematopoietic aging, independent of lung tissue aging, is sufficient to exacerbate fibrosis.
🔗 www.science.org/doi/10.1126/...

Holistic genetic barcoding reveals a lineage tree of tissue macrophage development Tissue macrophages are crucial for organ development and homeostasis, yet the developmental routes leading to tissue macrophages remain controversial. By combining unbiased Polylox barcoding with comp...

#macrophage #barcoding 🤯 Time to get rid of the "fetal liver monocyte" origin for resident macrophages?!? Congrats to the Rodewald lab for this work!
www.biorxiv.org/content/10.1...

REVIEW: Approaches to investigate tissue-resident innate lymphocytes metabolism at the single-cell level
www.nature.com/articles/s41...
@davidfinlaytcd.bsky.social