Spreading of inflammation: the skin-joint axis

The spread of inflammation from the skin to the joints is a key issue in the pathogenesis of psoriatic arthritis (PsA). Psoriasis (PsO), one of the most common skin diseases, usually precedes joint manifestations, suggesting skin-joint disease spread, which occurs in about 30% of psoriasis patients. Until now, it has been unclear why the inflammatory process remains restricted to the skin in some patients with PsO, whereas it spreads to tendons and joints in others. Using a preclinical model of PsA, we aimed to elucidate the skin-joint axis, i.e. the spread of psoriatic inflammation from the skin to the joints. KAEDE transgenic mice expressing a photo-convertible fluorescent reporter were used to assess cell trafficking from inflamed skin to other organs in the mouse model of IL-23 overexpression (IL-23OE) induced PsA. Psoriatic skin lesions were irradiated with UV light to induce the photoswitch from KAEDE-GREEN to KAEDE-RED. Migrating cells were characterised by scRNAseq. Overall design: Stromal and immune cells from synovial joints and skin were isolated by fluorescence-activated cell sorting from minicircle-induced IL-23 overexpression on day 7. Two libraries were generated corresponding to either Balb/c or C67BL/6 background. Viable CD45+ Ly6G- and viable CD45- were isolated and labelled with hashtag antibodies against CD45 and B2m. Please note that processed data genated from both GEX and HTO are linked to the corresponding *GEX sample records.