Figure 1.

Major effector cells and signaling pathways in the immunopathogenesis of psoriasis. The immunopathogenesis of psoriasis involves a complex inflammatory cascade, which is initially triggered by innate immune cells (keratinocytes, dendritic cells, NKT cells, macrophages). At the same time, the disease progresses and is maintained by their interaction with adaptive immune cells (T lymphocytes). The central mechanism of the disease is the IL-23/Th17 axis, whose executive cytokines IL-22 and IL-17A/F lead to keratinocyte proliferation, production of proinflammatory cytokines, chemokines and AMP, and the formation of a positive feedback loop, which maintains the inflammatory process. Cytokines in cells activate signaling and transcription pathways (cAMP, JAK-STAT), which achieve increased transcription of messenger genes and cytokines involved in the disease pathogenesis. Adapted from: [36].