Table 1. Pathogenesis of Psoriasis
PathwayProducerAction in Psoriasis
TNF-α (over expressed in psoriasis)5Macrophages, T cells, mast cells, granulocytes, natural killer cells, fibroblasts, neurons, keratinocytes, and smooth muscle cells5Increases the release of cytokines by lymphocytes and chemokines by macrophages6
Increases expression of adhesion molecules attracting neutrophils and macrophages to the lesions by activation of the vascular endothelium6
Induces keratinocyte and endothelial cell neovascularization stimulating the inflammatory process6
IL-12/23 (upregulated in psoriasis)7IL-12 promotes the differentiation of naive CD4+ T lymphocytes to Th1 cells.7
IL-12 triggers the specialization of CD4 and CD8 T lymphocytes by major histocompatibility complex class I and II, respectively, via antigen-presenting cells, which convert CD4+ cells into Th cells and CD8+ into cytotoxic T cells.6 As a result, TNF- α, IL-2, interferon-γ, and other cytokines are produced.6
Th17Th17 cells produce IL-17, a potent proinflammatory cytokineIl-17 directly perpetuates further inflammation of the keratinocyte, but it also indirectly stimulates production of IL-6.8
  • IL, interleukin; Th, T helper; TNF, tumor necrosis factor.