期刊連結：http://www.gouthyperuricemia.com

Purpose: Gout is characterized as an inflammatory arthritic disorder. The causal agent of gout has been extensively studied, but the detailed immune response underlying gout is still unclear. In this review, we will summarize the innate and adaptive immune responses in gout.
Findings: Both innate and adaptive immunity are involved in gouty inflammation. There are three major signaling pathways regulating innate immunity in gouty inflammation, including Toll-like receptors (TLRs)-myeloid differentiation factor 88 (MyD88) dependent nuclear factor-kappa B (NF-κB) pathway, NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome pathway, and interleukin-1 receptor (IL-1R)-MyD88 signaling pathway. Additionally, in adaptive immunity, T cells, including T helper 17 (Th17) cells, and B cells also have been proven to contribute to gouty inflammation.
Conclusion: Accumulated studies have linked both innate and adaptive immunity to gouty inflammation. However, there still are contradictory findings in the understanding of gouty inflammation, and the detailed mechanisms of immunity in gout require further investigations.