Unit of Rheumatology, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Eur J Immunol. 2012 Sep;42(9):2274-84. doi: 10.1002/eji.201242653.
Systemic autoimmune diseases such as systemic lupus erythematosus are type I IFN-driven diseases with exaggerated B-cell responses and autoantibody production. Th17 cells, a T-helper-cell subset with high inflammatory capacity, was initially discovered and characterized in the context of experimental autoimmune encephalomyelitis - an animal model of multiple sclerosis. There is now emerging evidence that Th17 cells, and more generally IL-17 and IL-17-producing cells, may play a role in the pathogenesis of type I IFN-driven systemic autoimmune diseases such as lupus. Here, we review the different studies suggesting a role for IL-17 and IL-17-producing cells in systemic autoimmune diseases, both in humans and in animal models, and we consider the possible mechanisms by which these cells may contribute to disease. We also discuss the hypothesis that type I IFN and IL-17 act in concert to sustain and amplify autoimmune and inflammatory responses, making them a dangerous combination involved in the pathogenesis of systemic autoimmune diseases.
系统性自身免疫性疾病，如系统性红斑狼疮，是一类由 I 型干扰素驱动的疾病，具有过度的 B 细胞反应和自身抗体产生。Th17 细胞是一种具有高炎症能力的辅助性 T 细胞亚群，最初在实验性自身免疫性脑脊髓炎（多发性硬化症的动物模型）的背景下被发现和描述。现在有越来越多的证据表明，Th17 细胞，以及更普遍的 IL-17 和产生 IL-17 的细胞，可能在 I 型干扰素驱动的系统性自身免疫性疾病（如狼疮）的发病机制中发挥作用。在这里，我们回顾了不同的研究，这些研究表明 IL-17 和产生 IL-17 的细胞在人类和动物模型中的系统性自身免疫性疾病中可能发挥作用，并考虑了这些细胞可能导致疾病的可能机制。我们还讨论了 I 型干扰素和 IL-17 协同作用以维持和放大自身免疫和炎症反应的假设，使它们成为参与系统性自身免疫性疾病发病机制的危险组合。
