Ferraccioli Gianfranco, Gremese Elisa
Institute of Rheumatology, School of Medicine, Catholic University of the Sacred Heart, Rome, Italy.
J Rheumatol Suppl. 2012 Jul;89:94-6. doi: 10.3899/jrheum.120255.
Understanding the biology of inflammation occurring at the entheseal-bone insertion has led to a better knowledge of the main drivers of inflammation in spondyloarthropathies. The clinical efficacy of tumor necrosis factor-α (TNF-α) blockers strongly supports the idea that TNF-α is a key molecule. Yet 40% of patients do not respond appropriately, indicating that other pathways are likely involved in these illnesses. Targeting T cells through a blockade of costimulating (CD28) molecules does not help, and in experimental models of sacroiliitis, targeting interleukin 6 (IL-6) did not provide any useful evidence. Immunohistological and functional data suggest that B cells, Th17, or IL-17A might be important, and indeed preliminary data concerning drugs targeting B cells and IL-17A seem to suggest clinical benefits.
对发生于附着点-骨插入处的炎症生物学的理解，使人们对脊柱关节炎炎症的主要驱动因素有了更深入的认识。肿瘤坏死因子-α（TNF-α）阻滞剂的临床疗效有力地支持了TNF-α是关键分子这一观点。然而，40%的患者并无适当反应，这表明其他途径可能也参与了这些疾病。通过阻断共刺激（CD28）分子来靶向T细胞并无帮助，并且在骶髂关节炎的实验模型中，靶向白细胞介素6（IL-6）也未提供任何有用证据。免疫组织学和功能数据表明B细胞、Th17或IL-17A可能很重要，事实上，有关靶向B细胞和IL-17A的药物的初步数据似乎显示出临床益处。
