PSORIASIS, THE ROLE OF INFLAMMATORY CYTOKINES (IL-17, TNF-α) IN PATHOGENESIS

Abstract

Psoriasis is a chronic inflammatory skin disease of autoimmune nature, characterized by accelerated keratinocyte proliferation, impairment of the epidermal barrier function, and systemic inflammation. Modern studies confirm that pro-inflammatory cytokines—particularly interleukin-17 (IL-17) and tumor necrosis factor alpha (TNF-α)—play a key role in the pathogenesis of psoriasis. IL-17, produced predominantly by Th17 cells, stimulates keratinocytes to express antimicrobial peptides, chemokines, and other inflammatory mediators, thereby creating a self-sustaining cycle of immune activation. TNF-α, secreted by macrophages and dendritic cells, enhances the production of IL-1, IL-6, and IL-23, which further activates the Th17 pathway and contributes to chronic inflammation in the dermis and epidermis. Understanding the molecular mechanisms mediated by IL-17 and TNF-α has formed the basis for the development of targeted biological therapeutic strategies. Biological agents blocking TNF-α (adalimumab, etanercept) and IL-17 (secukinumab, ixekizumab) have demonstrated high efficacy in reducing the severity of skin lesions, decreasing inflammatory activity, and improving patients’ quality of life. The modern approach to psoriasis treatment involves individualization of therapy based on the patient’s cytokine profile, allowing prediction of response to biological therapy and optimization of drug selection. Recent studies highlight the need to integrate molecular diagnostics, monitoring of inflammatory markers, and biological treatment methods, opening new prospects for achieving sustained remission, minimizing systemic adverse effects, and improving disease prognosis. Thus, the role of IL-17 and TNF-α in the pathogenesis of psoriasis is fundamental, and targeted therapy against these cytokines represents the current standard of care for patients with moderate to severe disease.