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

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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-2K^d (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/6 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-2K^d (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.
新潟大学の論文
2002-11-10

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

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