NEWS

NEW ACCEPTED PUBLICATION 

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Our lab has been investigating how obesity alters immune function at the level of blood stem cells. In this study, we uncovered a key mechanism by which diet-induced obesity leads to persistent inflammation and dysregulated myelopoiesis.
🔍 Key findings:
Obesity increases oxidative stress in hematopoietic stem and progenitor cells (HSPCs), which elevates H3K4me3, an epigenetic mark associated with active gene expression.
This reprogramming leads to chronic inflammation and impaired tissue recovery, even when these altered HSPCs are transferred into lean recipients.
Using CUT&Tag epigenomic profiling, we identified H3K4me3 enrichment at inflammatory and cell cycle genes like Tlr4 and E2F targets.
Notably, Cyclosporine A treatment ex vivo mitigated oxidative stress and normalized H3K4me3 levels in HSPCs, offering a potential therapeutic angle.
🧠 This work deepens our understanding of how metabolic disease drives long-term immune reprogramming and opens up avenues for targeting immune dysfunction in obesity-related conditions.
🙏 Grateful to my team and collaborators for their dedication and insight!
📄 Title: Diet-induced Obesity Induces Oxidative Stress and Enhances H3K4me3 Levels, Driving Non-resolving Inflammation and Myelopoiesis in Hematopoietic Stem and Progenitor Cells
📚 Journal of Immunology
🔗 It has been accepted, and a link will be available soon.