Pathophysiological roles of innate immune cells in psoriasis

Psoriasis is a chronic inflammatory skin disorder characterized by complex interactions between the innate and adaptive immune systems.Although the IL-23/Th17 axis and T cell-mediated immunity have been central to our understanding of disease pathogenesis, accumulating evidence underscores the pivotal contributions of innate immune cells, particularly in the initiation and amplification of inflammation.Neutrophils, macrophages, dendritic cells, mast cells, natural killer (NK) cells, natural killer T (NKT) cells, T cells, and innate lymphoid cells (ILCs) promote psoriatic inflammation by secreting pro-inflammatory cytokines, activating keratinocytes, and orchestrating crosstalk with adaptive immunity.These cells not only sustain the inflammatory microenvironment but also represent promising therapeutic targets.Both previously investigated and emerging therapeutic strategies-such as Tolllike receptor (TLR) antagonists, CXCR2 inhibitors, and CD1-targeting antibodies-highlight the growing clinical significance of modulating innate immune pathways in psoriasis.A more comprehensive understanding of these mechanisms may facilitate the development of synergistic treatments that enhance or complement existing therapies.