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Skin-derived G-CSF activates pathological granulopoiesis upon psoriasis
Tomson Kosasih1, Tatsuya Morishima1,2, Sohyeon Lee3
1Laboratory of Stem Cell Stress, International Research Center for Medical Sciences (IRCMS), Kumamoto University, Kumamoto, 860-811, Japan.
EMBO Molecular Medicine
|June 16, 2026
Summary
Neutrophils play a key role in psoriasis pathogenesis by accumulating in the skin. Targeting this neutrophil accumulation, driven by skin-bone marrow communication, may offer a new therapeutic strategy for psoriasis.
Area of Science:
- Immunology
- Dermatology
- Pathogenesis research
Background:
- Psoriasis is an inflammatory skin condition driven by T cell cytokines.
- Current treatments targeting key cytokines show limitations, suggesting other immune cells contribute.
- Neutrophils, crucial innate immune cells, are implicated in psoriasis pathogenesis.
Purpose of the Study:
- To investigate the role of neutrophils in psoriasis.
- To elucidate the mechanism of neutrophil recruitment and accumulation in psoriatic skin.
- To explore potential therapeutic strategies targeting neutrophil involvement in psoriasis.
Main Methods:
- Induction of psoriasis in a model system.
- Analysis of endothelial cell activation and G-CSF production.
- Neutrophil depletion studies and granulopoiesis inhibition.
- Reanalysis of public RNA-sequencing data from human psoriasis patients.
Main Results:
- Psoriasis induction activates skin endothelial cells to produce G-CSF.
- G-CSF promotes emergency granulopoiesis in bone marrow and neutrophil accumulation in the skin.
- Neutrophil depletion or inhibition of granulopoiesis reduces skin neutrophil burden and mitigates psoriasis.
- The observed mechanism is conserved in human psoriasis.
Conclusions:
- Neutrophils are critical players in psoriatic skin inflammation.
- A pathological crosstalk between skin and bone marrow, mediated by G-CSF, drives neutrophil accumulation.
- Targeting this cross-organ communication presents a potential therapeutic avenue for psoriasis.
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