Th9-arterial endothelial cell crosstalk promotes psoriatic atherosclerosis
Authors' conclusion
These findings suggest the Th9high state may represent a novel psoriatic ASCVD endotype that could be targeted using precision approaches to prevent ASCVD in at-risk individuals.
Study context
- Population
- Patients with psoriasis; murine models of psoriatic atherogenesis; primary human aortic endothelial cells
Methodological detailshuman cohort with coronary CT angiography, murine models (imiquimod-ApoE-/-, IL-23-ApoE-/-, Card14ΔE138-ApoE-/-), IL-9 blockade, global and endothelial-specific Il9r deletion, primary human aortic endothelial cells
- Human cohort with coronary CT angiography
- Murine models (imiquimod-ApoE-/-, IL-23-ApoE-/-, Card14ΔE138-ApoE-/-)
- IL-9 blockade
- Global and endothelial-specific Il9r deletion
- Primary human aortic endothelial cells
Main finding
As reported in the abstract
- Expansion of IL-9-producing T helper cells (Th9) significantly associated with high-risk radiographic atherosclerotic cardiovascular disease (ASCVD) in patients with psoriasis
- Th9 cells poised to migrate to coronary vessels and identified in human atherosclerotic plaque from individuals with psoriasis
- Murine inflammatory atherogenesis prevented by IL-9 blockade and by endothelial IL-9R deletion
- In human arterial endothelial cells, IL-9R/STAT3 signalling promoted endothelial dysfunction (adhesion, activation, angiogenesis, release of leukocyte chemoattractants)
Original publication
Th9-arterial endothelial cell crosstalk promotes psoriatic atherosclerosis. Ann Rheum Dis. Published 13 December 2025. doi:10.
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