Systemic CSF1R Targeting Depletes Pathogenic MPS Bubs and Ameliorates Psoriasis via PPARα-mediated Resolution.

ABSTRACT: Rationale: Psoriasis features persistent activation of the mononuclear phagocyte system (MPS), yet the subset-specific pathogenic roles of colony-stimulating factor 1 receptor (CSF1R) remain undefined. We aimed to identify pathogenic CSF1R^high MPS subsets, characterize their ligand-receptor circuits, and define the CSF1R-PPARα axis in disease pathogenesis. Methods: By integrating human single-cell and spatial transcriptomics with murine imiquimod (IMQ)-induced psoriasis models, we employed genetic and pharmacologic interventions to achieve our aims. Results: We found a pathologic CSF1R^high MPS population was selectively expanded, forming localized cytokine hubs enriched for TNF-α, IL-1β, and IL-23. Ligand mapping showed CSF1 upregulation amplified

SUBMITTER: Lin ZJ 

PROVIDER: S-EPMC12905821 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature