Immune and inflammatory mechanisms and therapeutic targets of gout: An update

•We found that gout is closely related to the activation of immune cells. Macrophages and neutrophils are involved in the formation and resolution of gout inflammation and the occurrence of complications through a variety of pathways.•We found that the interleukin-1 family plays an important role in gout inflammation. The interaction between inflammatory factors causes them to play different roles in different pathological conditions, change the phenotype of immune cells, and regulate the inflammatory microenvironment in the joint.•We found that studies on drugs for gout inflammation began to increase recently. In addition to effectively reducing uric acid, more and more studies have focused on the management of inflammation in gout. Targeted therapy of gout inflammation may be a new direction in the future. Gout is an autoimmune disease characterized by acute or chronic inflammation and damage to bone joints induced due to the precipitation of monosodium urate (MSU) crystals. In recent years, with the continuous development of animal models and ongoing clinical investigations, more immune cells and inflammatory factors have been found to play roles in gouty inflammation. The inflammatory network involved in gout has been discovered, providing a new perspective from which to develop targeted therapy for gouty inflammation. Studies have shown that neutrophil macrophages and T lymphocytes play important roles in the pathogenesis and resolution of gout, and some inflammatory cytokines, such as those in the interleukin-1 (IL-1) family, have been shown to play anti-inflammatory or proinflammatory roles in gouty inflammation, but the mechanisms underlying their roles are unclear. In this review, we explore the roles of inflammatory cytokines, inflammasomes and immune cells in the course of gout development and the research status of therapeutic drugs used for inflammation to provide insights into future targeted therapy for gouty inflammation and the direction of gout pathogenesis research.