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免疫抑制分子TRAILによる自己免疫疾患の制御機構に関する研究
http://hdl.handle.net/2298/21641
http://hdl.handle.net/2298/2164128c135bd-9528-4a46-8527-541dc4d70df6
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
22-1771.pdf (1.1 MB)
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| Item type | 学位論文 / Thesis or Dissertation(1) | |||||||||||
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| 公開日 | 2011-10-03 | |||||||||||
| タイトル | ||||||||||||
| タイトル | The immunoregulatory effect of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) | |||||||||||
| 言語 | en | |||||||||||
| タイトル | ||||||||||||
| タイトル | 免疫抑制分子TRAILによる自己免疫疾患の制御機構に関する研究 | |||||||||||
| 言語 | ja | |||||||||||
| タイトル | ||||||||||||
| タイトル | メンエキ セイギョ ブンシ TRAIL ニ ヨル ジコ メンエキ シッカン ノ セイギョ キコウ ニ カンスル ケンキュウ | |||||||||||
| 言語 | ja-Kana | |||||||||||
| 言語 | ||||||||||||
| 言語 | eng | |||||||||||
| 資源タイプ | ||||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_46ec | |||||||||||
| 資源タイプ | thesis | |||||||||||
| 著者 |
池田, 徳典
× 池田, 徳典
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| 内容記述 | ||||||||||||
| 内容記述 | Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) is known to play a pivotal role in the inhibition of autoimmune disease. We previously reported a disease-preventive effect of embryonic stem cell-derived dendritic cells (ES-DC) genetically engineered to express TRAIL along with a myelin antigen, MOG, on experimental autoimmune encephalomyelitis (EAE), and also suggested that CD4+CD25+ regulatory T (Treg) cells were involved in mediating this preventive effect. In the current study, we investigated the effect of TRAIL on Treg cells as well as conventional T cells, using TRAIL-deficient mice. Upon induction of EAE, TRAIL-deficient mice showed more severe clinical symptoms, a higher frequency of IFN-γ-producing CD4+ T (Th1) cells, and a lower frequency of CD4+Foxp3+ Treg cells than wild type mice. In vitro, conventional T cells stimulated by bone marrow-derived DC (BM-DC) from TRAIL-deficient mice showed a higher magnitude of proliferation than those stimulated by BM-DC from wild type mice. In contrast, TRAIL expressed on the stimulator BM-DC enhanced the proliferative response of CD4+CD25+ Treg cells in the culture. The functional TRAIL-receptor, mDR5, was expressed in both conventional T cells and Treg cells upon stimulation. On the other hand, the decoy receptor, mDc-TRAIL-R1 was slightly expressed only on CD4+CD25+ Treg cells. Therefore, the distinct effects of TRAIL may be due to differences in the mDc-TRAIL-R1-expreesion or the signaling pathways down-stream of mDR5 between the two T cell subsets. Our data suggests that TRAIL suppresses autoimmunity by two mechanisms; one is the inhibition of Th1 cells and the other is the promotion of Treg cells. | |||||||||||
| 書誌情報 |
発行年 2011-03-25 |
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| 著者版フラグ | ||||||||||||
| 出版タイプ | VoR | |||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||||
| 日本十進分類法 | ||||||||||||
| 主題 | 377.5 | |||||||||||
| 出版者 | ||||||||||||
| 出版者 | 熊本大学 | |||||||||||
| 言語 | ja | |||||||||||
| 学位名 | ||||||||||||
| 学位名 | 博士（医学）(ja) | |||||||||||
| 学位授与機関 | ||||||||||||
| 学位授与機関名 | 熊本大学 | |||||||||||
| 学位授与年月日 | ||||||||||||
| 学位授与年月日 | 2011-03-25 | |||||||||||
| 学位授与番号 | ||||||||||||
| 学位授与番号 | 甲第1771号 | |||||||||||
| コメント | ||||||||||||
| 値 | 熊本大学大学院医学教育部 臨床医科学専攻 | |||||||||||
| 学位番号 | ||||||||||||
| 値 | 甲博医第1771号 | |||||||||||
