IL-6 as a Druggable Target in Psoriasis: Focus on Pustular Variants

Figure 2

IL-17/IL-6 axis in the pathogenesis of pustular psoriasis. Both innate (gamma/delta T cells, neutrophils, and macrophages) and adaptive (Th17 cells) immunities contribute to cutaneous IL-17 production. Macrophages, conventional DCs, and slan-DCs respond to IL-17 by releasing IL-6, which in turn plays a key role in neutrophils recruitment and pustules formation; additional IL-6-dependent effects include reinforcement of Th1/Th17 inflammatory cytokines production, facilitation of IL-22-mediated epidermal hyperplasia, and naive CD4+ T cells differentiation into Th17. Activated keratinocytes amplify the IL-17/IL-6 axis by producing IL-6, recruiting Th17 cells through CCL20, and inducing neutrophils chemotaxis via IL-8 and MCP-1. DCs: dendritic cells; IL: interleukin; KCs: keratinocytes; M/Ms: monocytes/macrophages; PMNs: neutrophils; Th17: T helper 17 cells.