Okiyama Naoko, Hasegawa Hisanori, Oida Takatoku, Hirata Shinya, Yokozeki Hiroo, Fujimoto Manabu, Miyasaka Nobuyuki, Kohsaka Hitoshi
Department of Rheumatology, Tokyo Medical and Dental University (TMDU), Bunkyo-ku, Tokyo 113-8519, Japan Department of Dermatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Bunkyo-ku, Tokyo 113-8519, Japan Japan Society for the Promotion of Science, Tokyo 102-0083, Japan Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama, Kanagawa 230-0045, Japan Department of Dermatology, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibarakii 305-8575, Japan.
Department of Rheumatology, Tokyo Medical and Dental University (TMDU), Bunkyo-ku, Tokyo 113-8519, Japan.
Int Immunol. 2015 Jul;27(7):327-32. doi: 10.1093/intimm/dxv001. Epub 2015 Jan 10.
It is suggested that polymyositis, an autoimmune inflammatory myopathy, is mediated by autoaggressive CD8 T cells. Skeletal muscle C protein is a self-antigen that induces C protein-induced myositis, a murine model of polymyositis. To establish a new murine model of myositis inducible with a single CD8 T-cell epitope peptide that derives from the C protein, three internet-based prediction systems were employed to identify 24 candidate peptides of the immunogenic fragment of the C protein and bind theoretically to major histocompatibility complex class I molecules of C57BL/6 (B6) mice. RMA-S cell assay revealed that a HILIYSDV peptide, amino acid position 399-406 of the C protein, had the highest affinity to the H2-K(b) molecules. Transfer of mature bone marrow-derived dendritic cells pulsed with HILIYSDV induced myositis in naive B6 mice. This myositis was suppressed by anti-CD8-depleting antibodies but not by anti-CD4-depleting antibodies. Because this myositis model is mediated by CD8 T cells independently of CD4 T cells, it should be a useful tool to investigate pathology of polymyositis and develop therapies targeting CD8 T cells.
有人提出,多发性肌炎作为一种自身免疫性炎性肌病,是由具有自身攻击性的CD8 T细胞介导的。骨骼肌C蛋白是一种自身抗原,可诱发C蛋白诱导性肌炎,这是一种多发性肌炎的小鼠模型。为了建立一种可由源自C蛋白的单一CD8 T细胞表位肽诱导的新型肌炎小鼠模型,使用了三个基于互联网的预测系统来识别C蛋白免疫原性片段的24个候选肽,并从理论上与C57BL/6(B6)小鼠的主要组织相容性复合体I类分子结合。RMA-S细胞试验表明,C蛋白氨基酸位置399 - 406的HILIYSDV肽与H2-K(b)分子具有最高亲和力。用HILIYSDV脉冲处理的成熟骨髓来源树突状细胞转移到未接触过抗原的B6小鼠中可诱发肌炎。这种肌炎可被抗CD8耗竭抗体抑制,但不能被抗CD4耗竭抗体抑制。由于这种肌炎模型是由CD8 T细胞独立于CD4 T细胞介导的,它应该是研究多发性肌炎病理和开发针对CD8 T细胞疗法的有用工具。