Psoriatic arthritis (PsA) is part of a group of closely related clinical phenotypes (‘psoriatic disease’) that is defined by shared molecular pathogenesis resulting in excessive, prolonged inflammation in the various tissues affected, such as the skin, the entheses or the joints. Psoriatic disease comprises a set of specific drivers that promote an aberrant immune response and the consequent development of chronic disease that necessitates therapeutic intervention. These drivers include genetic, biomechanical, metabolic and microbial factors that facilitate a robust and continuous mobilization, trafficking and homing of immune cells into the target tissues. The role of genetic variants involved in the immune response, the contribution of mechanical factors triggering an exaggerated inflammatory response (mechanoinflammation), the impact of adipose tissue and altered lipid metabolism and the influence of intestinal dysbiosis in the disease process are discussed. Furthermore, the role of key cytokines, such as IL-23, IL-17 and TNF, in orchestrating the various phases of the inflammatory disease process and as therapeutic targets in PsA is reviewed. Finally, the nature and the mechanisms of inflammatory tissue responses inherent to PsA are summarized.

银屑病关节炎 (PsA) 是一组密切相关的临床表型（“银屑病”）的一部分，其定义为共同的分子发病机制导致各种受影响组织（如皮肤、附着点或关节）出现过度、长期的炎症. 银屑病包括一组特定的驱动因素，这些驱动因素会促进异常的免疫反应以及随之而来的需要治疗干预的慢性疾病的发展。这些驱动因素包括遗传、生物力学、代谢和微生物因素，这些因素有助于免疫细胞稳健和持续地动员、运输和归巢到目标组织中。遗传变异在免疫反应中的作用，机械因素引发过度炎症反应（机械炎症）的作用，讨论了脂肪组织和脂质代谢改变的影响以及肠道生态失调在疾病过程中的影响。此外，还回顾了关键细胞因子（如 IL-23、IL-17 和 TNF）在协调炎症性疾病过程的各个阶段以及作为 PsA 治疗靶点中的作用。最后，总结了 PsA 固有的炎症组织反应的性质和机制。