In psoriasis models, the CCR10–CCL27 axis restrains disease: CCR10 skin ILCs arise in skin-draining lymph nodes (LNs) but decline under inflammation/homeostatic stress while CCR10 deficient ILCs expand in LNs and skin (47–49), limiting hyperactivation of IL-17A and IL-22 secreting cells as αβT, γδT, and Th17 cells, while impaired signaling exacerbates pathology (47, 48). This evidence concerns the gene CCR10 and psoriasis.