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首页> 外文期刊>Arthritis & Rheumatism >The adaptor protein CIKS/ACT1 is necessary for collagen-induced arthritis, and it contributes to the production of collagen-specific antibody
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The adaptor protein CIKS/ACT1 is necessary for collagen-induced arthritis, and it contributes to the production of collagen-specific antibody

机译：衔接蛋白CIKS / ACT1对于胶原诱导的关节炎是必需的，并且它有助于胶原特异性抗体的产生

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ObjectiveCIKS/ACT1 is an adaptor molecule that is necessary for signaling by members of the interleukin-17 cytokine family. The aim of this study was to determine whether this adaptor is required for the initiation of collagen-induced arthritis (CIA). If it is required, then CIKS-mediated signaling could be a potential target for therapeutic intervention in patients with rheumatoid arthritis (RA).MethodsCIA model studies were performed with CIKS-deficient and CIKS-sufficient mice on an otherwise wild-type (WT) C57BL/6 background or on a C57BL/6 background lacking Fc receptor IIb (FcRIIb). In addition, collagen antibody–induced arthritis (CAIA) studies were performed in WT and CIKS-deficient mice. Pathologic changes of arthritis were evaluated by visual inspection of the paws, by histochemical analysis of tissue sections, and by measurements of collagen-specific antibodies.ResultsPathologic changes of CIA were readily induced in WT mice, with exacerbation of the changes in FcRIIb-deficient mice. In contrast, CIKS-deficient mice were protected from all aspects of CIA pathology, even on an FcRIIb-deficient background. The absence of CIKS completely prevented neutrophil infiltration into joints, bone erosion, and cartilage damage; furthermore, the production of type II collagen (CII)–specific antibodies was reduced. In contrast to the CIA model, CIKS-deficient mice in the CAIA model remained susceptible to arthritis.ConclusionCIKS-mediated signaling is necessary for the pathogenesis of CIA, but not CAIA. These findings suggest critical functions of CIKS during the development of arthritis in the CIA model, including in the formation of CII antibodies, and they mark the CIKS adaptor as a potential therapeutic target in RA.
机译：ObjectiveCIKS / ACT1是介导白介素-17细胞因子家族成员信号传导所必需的衔接子分子。这项研究的目的是确定是否需要这种适配器来引发胶原蛋白诱发的关节炎（CIA）。如果需要，CIKS介导的信号传导可能成为类风湿关节炎（RA）患者治疗干预的潜在靶点。方法用CIKS缺陷小鼠和CIKS充分小鼠对CIA模型进行研究C57BL / 6背景或缺少Fc受体IIb（FcRIIb）的C57BL / 6背景。此外，还对野生型和CIKS缺陷型小鼠进行了胶原抗体诱导的关节炎（CAIA）研究。通过肉眼检查爪，通过组织切片的组织化学分析以及通过测量胶原特异性抗体来评估关节炎的病理学变化。 。相反，即使在FcRIIb缺乏的背景下，CIKS缺陷的小鼠也不受CIA病理学所有方面的保护。 CIKS的缺乏完全阻止了中性粒细胞浸润到关节，骨侵蚀和软骨损伤。此外，减少了II型胶原（CII）特异性抗体的产生。与CIA模型相比，CAIA模型中CIKS缺陷型小鼠仍然易患关节炎。结论CIKS介导的信号转导对于CIA的发病机理是必需的，但对CAIA则不是。这些发现表明CIKS在CIA模型关节炎发展过程中的关键功能，包括在CII抗体的形成中，并且将CIKS衔接子标记为RA中潜在的治疗靶标。

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