Cho Wang Shik, Jang Eunkyeong, Kim Ho-Youn, Youn Jeehee
Department of Anatomy & Cell Biology, College of Medicine, Hanyang University, Seoul 04763, Korea.
Konkuk University Medical Center, Seoul 05030, Korea.
Immune Netw. 2016 Dec;16(6):366-372. doi: 10.4110/in.2016.16.6.366. Epub 2016 Dec 22.
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 Sca1 Thy1 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 Sca1 Thy1 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.
K/BxN血清可在正常小鼠中诱发关节炎,因为其中丰富的自身抗体会触发关节中的先天性炎症反应。为了确定白细胞介素-17(IL-17)是否参与血清诱导性关节炎的发病机制,我们给野生型小鼠和IL-17基因敲除小鼠注射K/BxN血清,并评估它们的关节炎症状。与野生型小鼠不同,IL-17基因敲除小鼠未表现出任何关节炎症状。IL-17主要由存在于炎症滑膜组织中的CD3⁺CD4⁻γδTCR⁺NK1.1⁻Sca1⁺Thy1⁺细胞产生。当用IL-23或含自身抗体的免疫复合物刺激从正常关节提取的滑膜细胞时,相当一部分Sca1⁺Thy1⁺细胞会产生IL-17。因此,我们鉴定出了一群新的产生IL-17的先天性滑膜细胞,它们在K/BxN血清诱导性关节炎的发展中起关键作用。