Core Viewpoint - The study identifies CCR7+ dendritic cells as the primary source of IL-23 in psoriasis, providing a cellular framework for developing therapies aimed at achieving long-term relief from psoriasis and related chronic inflammation [3][4][7]. Group 1: Research Findings - The research reveals that IL4I1+ CD200+ CCR7+ dendritic cells (CCR7+ DC) express both IL-23A and IL-12B, making them the main producers of IL-23 in psoriasis [4][7]. - CCR7+ DC can drive psoriasis relapse through a spatially organized "Th17 module," recruiting IL-17 producing CD161+ T cells and activating keratinocytes responsive to IL-17 [7][8]. - The absence of CCR7+ DC in mouse models completely inhibits IL-23 production, while forced expression of IL-23A in these cells induces psoriasis-like skin disease and arthritis [8]. Group 2: Implications for Therapy - The findings provide a cellular basis for developing therapies that can disrupt the persistent presence of IL-23, potentially leading to sustained relief from psoriasis and associated chronic inflammation [4][8].