Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Curr Opin Rheumatol. 2010 Sep;22(5):499-503. doi: 10.1097/BOR.0b013e32833c62b0.
Interleukin-17 (IL-17) has emerged as a key cytokine involved in the pathogenesis of autoimmune diseases. In this article, we review recently produced evidence obtained in patients and murine models of lupus that link increased IL-17 production with lupus pathology and discuss the potential roles IL-17 may play in the pathogenesis of systemic lupus erythematosus.
IL-17 may promote autoantibody production and IL-17-producing cells are found in afflicted organs in humans and lupus-prone mice. TH17 and CD3+CD4-CD8- cells are expanded in systemic lupus erythematosus patients and account for the increased production of IL-17. Genetic silencing of genes involved in the increased production of IL-17 in lupus-prone mice as well as treatment of mice with lupus using biologic agents that result in decreased IL-17 production leads invariably to disease mitigation.
The presented evidence strongly argues for the introduction of IL-17-suppressing biologics in the treatment of patients with systemic lupus erythematosus.
白细胞介素-17(IL-17)已成为参与自身免疫性疾病发病机制的关键细胞因子。本文综述了最近在狼疮患者和小鼠模型中获得的证据,这些证据将增加的 IL-17 产生与狼疮病理学联系起来,并讨论了 IL-17 在系统性红斑狼疮发病机制中可能发挥的作用。
IL-17 可能促进自身抗体的产生,并且在人类和狼疮易感小鼠的受累器官中发现了产生 IL-17 的细胞。TH17 和 CD3+CD4-CD8-细胞在系统性红斑狼疮患者中扩增,并导致 IL-17 的产生增加。狼疮易感小鼠中涉及增加 IL-17 产生的基因的遗传沉默,以及使用导致 IL-17 产生减少的生物制剂治疗狼疮小鼠,都不可避免地导致疾病缓解。
目前的证据强烈支持在系统性红斑狼疮患者的治疗中引入抑制 IL-17 的生物制剂。