In Spondyloarthropathies (SpA), a common group of immune-mediated diseases characterised by excessive inflammation of musculo-skeletal structures and extra-articular organs, T helper 17 (Th17) cells are widely considered the main drivers of the disease. Th17 are able to modulate their genes according to the immune environment: upon differentiation, they can adopt either housekeeping, anti-bacterial gene modules or inflammatory, pathogenic functions, and only the latter would mediate immune diseases, such as SpA. Experimental work aimed at characterising Th17 heterogeneity is largely performed on murine cells, for which the in vitro conditions conferring pathogenic potential have been identified and replicated. Interestingly, Th17 recognising different microorganisms are able to acquire specific cytokine signatures. An emerging area of research associates this heterogeneity to the preferential metabolic needs of the cell. In summary, the tissue environment could be determinant for the acquisition of pathogenetic features; this is particularly important at barrier sites, such as the intestine, considered one of the key target organs in SpA, and likely a site of immunological changes that initiate the disease. In this review, we briefly summarise genetic, environmental and metabolic factors that could explain how homeostatic, anti-microbial Th17 could turn into disease-causing cells in Spondyloarthritis.

脊柱关节病 (SpA) 是一组常见的以肌肉骨骼结构和关节外器官过度炎症为特征的免疫介导疾病，T 辅助 17 (Th17) 细胞被广泛认为是该疾病的主要驱动因素。Th17 能够根据免疫环境调节其基因：分化后，它们可以采用看家、抗菌基因模块或炎症、致病功能，只有后者才能介导免疫疾病，如 SpA。旨在表征 Th17 异质性的实验工作主要在鼠细胞上进行，为此体外已鉴定并复制了具有致病潜力的条件。有趣的是，识别不同微生物的 Th17 能够获得特定的细胞因子特征。一个新兴的研究领域将这种异质性与细胞的优先代谢需求联系起来。总之，组织环境可能是获取致病特征的决定因素；这在屏障部位尤其重要，例如肠道，被认为是 SpA 的关键靶器官之一，并且可能是引发疾病的免疫变化部位。在这篇综述中，我们简要总结了遗传、环境和代谢因素，这些因素可以解释稳态、抗微生物 Th17 如何在脊柱关节炎中转变为致病细胞。