Inflammatory Cytokines in Psoriatic Arthritis: Understanding Pathogenesis and Implications for Treatment

Psoriatic arthritis (PsA) is a persistent, inflammatory disease that affects individuals with psoriasis, arthritis, and enthesitis. Research has demonstrated that inflammatory cytokines such as tumor necrosis factor-alpha (TNF-& alpha;), interleukin-23 (IL-23), and interleukin-17 (IL-17) play a pivotal role in both the onset and progression of PsA. These cytokines are generated by activated immune cells and stimulate the attraction of inflammatory cells to the synovium and joint tissues, resulting in the deterioration of cartilage and bone. The blocking of these cytokines has become a successful treatment strategy for PsA, as biological drugs that inhibit TNF-& alpha;, IL-23, and IL-17 have demonstrated notable clinical benefits. The association between PsA and other types of inflammatory cytokines or chemokines, excluding TNF-& alpha;, IL-23, and IL-17, has been extensively investigated in numerous studies. These findings may provide a chance for the discovery of novel therapeutic agents targeting other molecules, distinct from the currently approved biologics and targeted synthetic disease-modifying anti-rheumatic drugs. In this review, we discuss the current understanding of the role of inflammatory cytokines in PsA pathogenesis and clinical implications of targeting these cytokines for PsA treatment.

Automated summary

Psoriatic arthritis (PsA) is a chronic inflammatory disease that affects individuals with psoriasis, arthritis, and enthesitis. Inflammatory cytokines, such as TNF-α, IL-23, and IL-17, play a crucial role in the onset and progression of PsA by attracting inflammatory cells to the joint tissues and causing cartilage and bone deterioration. Blocking these cytokines has shown significant clinical benefits, and further research is being conducted to explore other potential therapeutic targets for PsA treatment. This review discusses the current understanding of the role of inflammatory cytokines in PsA pathogenesis and the clinical implications of targeting these cytokines.