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Psoriasis initially affects the skin and then spreads to the joints. Here, we present a two-step process that coordinates the spread of inflammation from the skin to the joints. Psoriasis skin lesions were induced in light-convertible mice, and subsequent sequencing and computational characterization of joint skin-derived cells identified the CD2+ MHC-II+ CCR2+ bone marrow precursor population that builds a skin-derived bone marrow cell compartment within the joints. Single-cell cross-species reference maps and mitochondrial variation tracking showed that the human cell population was homologous. The interaction group analysis of the joints revealed that in the second step, the resident regulatory CD200+ fibroblasts regulate the initiation of CD2+ MHC-II+ CCR2+ bone marrow precursors, and subsequently regulate the IL-17 expression in T cells. Therefore, the spread of inflammation requires a unique migratory bone marrow lineage precursor population and a permitted local tissue environment, similar to tumor metastasis.
This study was published in Nature Immunology under the title "Skin-derived myeloid precursors and joint-resident fibroblasts spread psoriatic disease from skin to joints".
Reference: DOI: 10.1038/s41590-025-02351-z
