Understanding the complex mechanisms underlying a disorder such as spondyloarthritis (SpA) may benefit from studying animal models. Several suitable models have been developed, in particular to investigate the role of genetic factors predisposing to SpA, including HLA-B27, ERAP1, and genes related to the interleukin (IL)-23/IL-17 axis. One of the best examples of such research is the HLA-B27 transgenic rat model that fostered the emergence of original theories regarding HLA-B27 pathogenicity, including dysregulation of innate immunity, contribution of the adaptive immune system to chronic inflammation, and influence of the microbiota on disease development. Very recently, a new model of HLA-B27 transgenic Drosophila helped to expand further some of those theories in an unexpected direction involving the TGFβ/BMP family of mediators. On the other hand, several spontaneous, inducible, and/or genetically modified mouse models—including SKG mouse, TNF^ΔARE mouse and IL-23-inducible mouse model of SpA—have highlighted the importance of TNFα and IL-23/IL-17 axis in the development of SpA manifestations. Altogether, those animal models afford not only to study disease mechanism but also to investigate putative therapeutic targets.

了解诸如脊柱关节炎 (SpA) 等疾病的复杂机制可能会受益于动物模型的研究。已经开发了几种合适的模型，特别是研究易患 SpA 的遗传因素的作用，包括 HLA-B27、ERAP1和与白介素 (IL)-23/IL-17 轴相关的基因。此类研究的最佳例子之一是 HLA-B27 转基因大鼠模型，该模型促进了有关 HLA-B27 致病性的原始理论的出现，包括先天免疫失调、适应性免疫系统对慢性炎症的贡献以及微生物群的影响关于疾病的发展。最近，一种新的 HLA-B27 转基因果蝇模型有助于在涉及 TGFβ/BMP 介质家族的意想不到的方向上进一步扩展其中一些理论。另一方面，一些自发的、诱导型和/或转基因小鼠模型——包括 SKG 小鼠、TNF ^ΔARE小鼠和 IL-23 诱导型 SpA 小鼠模型——强调了 TNFα 和 IL-23/IL-17 的重要性轴在 SpA 表现的发展中。总之，这些动物模型不仅可以研究疾病机制，还可以研究推定的治疗靶点。