Spreading inflammation via the skin–joint axis – Immunology Research

Approximately one third of individuals with the inflammatory skin disease psoriasis go on to develop joint inflammation (psoriatic arthritis). Raimondo et al. wanted to understand the mechanism behind this spread. Now, reporting in Nature Immunology, they show that a population of myeloid precursor cells migrates from psoriatic skin to the joints. There, they can become inflammatory macrophages and cause joint disease, unless they encounter joint-resident regulatory CD200⁺ fibroblasts that keep them in check. The authors thus propose that a two-step process drives progression from psoriatic skin to joint disease; it requires migrating cells and a supportive microenvironment — similar to tumour metastasis.

Light-sheet microscopy and flow cytometry revealed that IL-23 overexpression induced robust leukocyte migration from psoriatic skin to ankle joints, at comparable levels in both the arthritis-susceptible BALB/c strain and the arthritis-resistant C57BL/6 strain. Surprisingly, myeloid cells (rather than T cells or B cells) dominated this trafficking, accounting for approximately 85% of migrated leukocytes.