Centre for Immunobiology, Institute for Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Curr Opin Rheumatol. 2013 Jul;25(4):440-7. doi: 10.1097/BOR.0b013e32836202dc.
The spondyloarthropathies (SpAs) are a group of interrelated inflammatory disorders with overlapping clinical features. Current SpA treatments only provide partial symptomatic and functional relief in a subgroup of patients. Consequently, there is a need to better understand the pathophysiology of SpA to develop more specific and effective treatments for these conditions.
Genetic and mechanistic evidence links SpA with inflammatory bowel disease (IBD) and psoriasis, and the symptoms of these diseases partially overlap. Regulatory T cells (Tregs) and dendritic cells control the adaptive immune response, and failures in their functions are likely to contribute to the establishment of chronic inflammation. The contributions of Tregs and dendritic cells to IBD and SpA have been assessed in both animal models of disease and patients.
Although defects in Tregs are important in psoriasis and in animal models of IBD, there is little evidence that they are important in SpA. However, data from animal models indicate that dendritic cells drive pathogenic T-cell responses, partly through the production of interleukin-23 (IL-23). Dendritic cells from SpA patients may also contribute to disease by producing IL-23, therefore supporting the differentiation of the Th17 cells that contribute to inflammation. The driving forces in SpA pathophysiology are now becoming clear; these data may lead to the development of novel therapies to target SpA and related inflammatory disorders.
脊柱关节炎（SpA）是一组具有重叠临床特征的相关炎症性疾病。目前的 SpA 治疗方法仅能为一部分患者提供部分症状和功能缓解。因此，需要更好地了解 SpA 的发病机制，以便为这些疾病开发更特异和有效的治疗方法。
遗传和机制证据将 SpA 与炎症性肠病（IBD）和银屑病联系起来，这些疾病的症状部分重叠。调节性 T 细胞（Tregs）和树突状细胞控制适应性免疫反应，其功能的失败可能导致慢性炎症的建立。Tregs 和树突状细胞在疾病的动物模型和患者中均被用于评估其对 IBD 和 SpA 的作用。
尽管 Tregs 的缺陷在银屑病和 IBD 的动物模型中很重要，但在 SpA 中几乎没有证据表明它们很重要。然而，来自动物模型的数据表明，树突状细胞驱动致病性 T 细胞反应，部分通过产生白细胞介素-23（IL-23）。来自 SpA 患者的树突状细胞也可能通过产生 IL-23 而导致疾病，从而支持有助于炎症的 Th17 细胞的分化。SpA 发病机制的驱动力现在已经变得清晰；这些数据可能导致开发针对 SpA 和相关炎症性疾病的新型治疗方法。
