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首页> 外文期刊>Arthritis & Rheumatism >Definitive engagement of cytotoxic CD8 T cells in C protein–induced myositis, a murine model of polymyositis
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Definitive engagement of cytotoxic CD8 T cells in C protein–induced myositis, a murine model of polymyositis

机译：在C蛋白诱导的肌炎（一种多发性肌炎的小鼠模型）中，细胞毒性CD8 T细胞的明确参与

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摘要

ObjectiveTo substantiate a pathogenic role of cytotoxic CD8 T cells in the development of a murine polymyositis model, C protein–induced myositis (CIM).MethodsBeta2-microglobulin–null mutant, perforin-null mutant, and wild-type (WT) C57BL/6 mice were immunized with skeletal muscle C protein fragments to provoke CIM. Regional lymph node CD8 or CD4 T cells stimulated with C protein–pulsed dendritic cells were transferred adoptively to naive mice. Inflammation and damage of the muscle tissues were evaluated histologically.ResultsThe incidence of myositis development was significantly lower in β2-microglobulin–null and perforin-null mutant mice compared with WT mice. Inflammation was less severe in mutant mice, and the incidence of muscle injury was reduced significantly. Adoptive transfer of lymph node T cells from mice with CIM induced myositis in naive recipient mice. The CD8 T cell–induced muscle injuries were significantly more severe than the CD4 T cell–induced muscle injuries.ConclusionPerforin-mediated cytotoxicity by CD8 T cells is definitively responsible for muscle injury in CIM.
机译：目的证实细胞毒性CD8 T细胞在鼠多肌炎模型（C蛋白诱导的肌炎（CIM））发展中的致病作用。方法β 2 -微球蛋白无效突变体，穿孔素无效突变体和野生型用骨骼肌C蛋白片段免疫2型（WT）C57BL / 6小鼠以引起CIM。用C蛋白脉冲树突状细胞刺激的区域淋巴结CD8或CD4 T细胞过继转移至幼稚小鼠。结果：与WT小鼠相比，β 2 -微球蛋白无效和穿孔素无效的突变小鼠的肌炎发生率明显降低。突变小鼠的炎症反应较轻，肌肉损伤的发生率显着降低。在幼稚的受体小鼠中过继转移具有CIM的小鼠的淋巴结T细胞诱导的肌炎。 CD8 T细胞引起的肌肉损伤比CD4 T细胞引起的肌肉损伤严重得多。结论CD8 T细胞的穿孔素介导的细胞毒性是CIM中肌肉损伤的最终原因。

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  • 来源
    《Arthritis & Rheumatism》 |2010年第10期|p.3088-3092|共5页
  • 作者

    Takahiko Sugihara; Naoko Okiyama; Mihoko Suzuki; Kuniko Kohyama; Yoh Matsumoto; Nobuyuki Miyasaka; Hitoshi Kohsaka;

  • 作者单位

    Tokyo Medical and Dental University, Tokyo, and Yokohama Institute, RIKEN, Yokohama, Japan;

    Tokyo Medical and Dental University, Tokyo, and Yokohama Institute, RIKEN, Yokohama, Japan;

    Tokyo Medical and Dental University, Tokyo, Japan;

    Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan;

    Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan;

    Tokyo Medical and Dental University, Tokyo, Japan;

    Tokyo Medical and Dental University, Tokyo, and Yokohama Institute, RIKEN, Yokohama, Japan;

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