@article{oai:niigata-u.repo.nii.ac.jp:00014007,
 author = {河内, 泉},
 issue = {11},
 journal = {新潟医学会雑誌, 新潟医学会雑誌},
 month = {Nov},
 note = {Polymyositis(PM) is an inflammatory muscle disease caused by autoimmune dysfunction, and considered to be caused by cytotoxic CD 8 T cells. To date no autoantigens have been identified. We attempted to induce an experimental allergic myositis (EAM) in BALB/c mice by inoculating syngeneic dendritic cells (DCs) presenting peptides that are expected to match the binding anchor motif of H-2Kd(BALB/c). We selected peptides that are abundantly expressed in skeletal muscle as the candidate antigens. Only when we inoculated syngeneic bone-marrow-derived DCs presenting pyruvate kinase M1/M2 peptide 464-472 in BALB/c mice, 41.7% of the mice (EAM) developed pathological changes in skeletal muscle compatible to human-PM. Under other conditions (when we inoculated DCs presenting sodium channel protein (skeletal muscle alpha-subunit) peptide 1264-1274 into BALB/c or C57BL mice, or DCs presenting pyruvate kinase M1/M2 peptide into C57BL/6 mice, there were no necrotizing and inflammatory lesions. Induction of EAM in the same manner as above also induced CTL activity against P815 cells with the pyruvate kinase M1/M2 peptide and syngeneic differentiated-cultured-myotubes without peptides by the chromium release assay. Consistent with the similarity of the binding anchor motifs of H-2Kd (BALB/c) and HLA A*2402, we found that pyruvate kinase M1/M2 peptide-specific and interferon γ-producing T lymphocytes existed in peripheral blood of human-PM with the HLA A*2402 allele by the enzyme linked immunospot (ELISPOT) assay. Therefore we concluded that pyruvate kinase M1/M2 peptide is a candidate autoantigen not only in BALB/c-EAM but also in human-PM with the HLA A*2402 allele.},
 pages = {546--565},
 title = {ヒト多発筋炎発症機構の研究 : 樹状細胞移植による実験的アレルギー性筋炎モデルマウスの解析をもとに},
 volume = {116},
 year = {2002}
}