K/BxN serum can induce arthritis in normal mice because of abundant autoantibodies that trigger an innate inflammatory response in joints. To determine whether IL-17 is involved in the pathogenesis of serum-induced arthritis, we injected wild-type and IL-17−/− mice with K/BxN serum and evaluated them for signs of arthritis. Unlike wild-type mice, IL-17−/− mice did not show any signs of arthritis. IL-17 was produced predominantly by CD3− CD4− γδTCR− NK1.1− Sca1int Thy1hi cells residing in the inflamed synovial tissue. When synovial cells extracted from normal joints were stimulated with IL-23 or autoantibody-containing immune complexes, a substantial fraction of Sca1int Thy1hi cells produced IL-17. Thus, we have identified a novel population of IL-17-producing innate synovial cells that play a crucial role in the development of K/BxN serum-induced arthritis.

中文翻译：

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表达白细胞介素 17 的先天滑膜细胞驱动 K/Bxn 血清诱导的关节炎

K/BxN 血清可诱发正常小鼠的关节炎，因为其自身抗体丰富，可触发关节的先天炎症反应。为了确定 IL-17 是否参与了血清诱导关节炎的发病机制，我们给野生型和 IL-17-/- 小鼠注射了 K/BxN 血清，并评估了它们的关节炎迹象。与野生型小鼠不同，IL-17-/- 小鼠没有表现出任何关节炎迹象。IL-17 主要由位于发炎滑膜组织中的 CD3-CD4-γδTCR-NK1.1-Sca1int Thy1hi 细胞产生。当从正常关节中提取的滑膜细胞用 IL-23 或含有自身抗体的免疫复合物刺激时，大部分 Sca1int Thy1hi 细胞会产生 IL-17。因此，