Figure 1. Pathogenesis of psoriasis.

Exposure to microbial or mechanical injury-induced damage leads to the activation of antigen-presenting cells (APCs), such as macrophages and dermal dendritic cells. The failure to maintain the skin barrier, often due to the deletion of late cornified envelope proteins 3C/3B, results in continuous exposure to these antigens. The interaction between APCs and T cells triggers the activation of Th1 and Th17 cells, mediated by IL-23. Subsequently, Th17 cells release IL-17 and IL-22, while Th1 cells produce tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ), perpetuating keratinocyte injury. This establishes a vicious positive feedback cycle exacerbating skin damage.