SerpApi.Org
Psoriasis is a chronic inflammatory skin disease affecting more than 60 million people worldwide, characterized by painful red patches, scaling and skin thickening. While existing biologic treatments largely focus on calming hyperactive T cells in the skin, complete disease resolution remains challenging.
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Now, a research team led by scientists at Kumamoto University has uncovered a hidden communication network between the skin and the bone marrow that drives psoriatic inflammation. Published in EMBO Molecular Medicine, the study highlights a crucial, previously underappreciated role for neutrophils—first-line immune defense cells—and proposes a promising new target for future therapies.
Skin-bone marrow pathological connection
A hallmark of psoriatic skin is the heavy accumulation of neutrophils, which form tiny microabscesses and exacerbate inflammation. Because these cells are naturally short-lived, the body must continuously replenish them through a process called granulopoiesis in the bone marrow.
Using an inducible psoriasis mouse model and advanced 3D intravital imaging, the Kumamoto University researchers discovered that local skin inflammation triggers a long-distance alarm. Specifically, skin-resident endothelial cells—the cells lining blood vessels—are activated by environmental triggers and begin producing high levels of granulocyte colony-stimulating factor (G-CSF).
This skin-derived G-CSF travels through the bloodstream to the bone marrow, triggering "emergency granulopoiesis" and generating a massive oversupply of inflammatory neutrophils. These newly minted neutrophils then travel back through expanded blood vessels to infiltrate the skin, where they produce high levels of reactive oxygen species (ROS) and interleukin-17A (IL-17A), worsening tissue damage.
Potential for combined therapies
When the research team blocked G-CSF signaling or depleted neutrophils using neutralizing antibodies, the burden of neutrophils in the skin plummeted, and both clinical and histological psoriasis symptoms were mitigated. Furthermore, reanalysis of public human patient databases and single-cell RNA sequencing confirmed that this skin-derived G-CSF mechanism is also active in human psoriasis.
"Our findings uncover a pathological cross-organ feedback loop between the skin and bone marrow," noted Professor Hitoshi Takizawa from the International Research Center for Medical Sciences (IRCMS) at Kumamoto University.
Because current biologic drugs primarily target adaptive immunity (like T-cell pathways) and offer limited control over neutrophil-driven inflammation, combining existing treatments with therapies that block this G-CSF/neutrophil axis could pave the way for more comprehensive and long-lasting relief for people with psoriasis.
More information: Tomson Kosasih et al, Skin-derived G-CSF activates pathological granulopoiesis upon psoriasis, EMBO Molecular Medicine (2026). DOI: 10.1038/s44321-026-00456-y
Provided by Kumamoto University
This story was originally published on Medical Xpress.
