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The immunoregulatory effect of tumor necrosis factor-related apoptosis inducing ligand (TRAIL)
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 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ | thesis | |||||
| 著者 |
池田, 徳典
× 池田, 徳典 |
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| 別言語の著者 |
Ikeda, Tokunori
× Ikeda, Tokunori |
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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 | |||||
| フォーマット | ||||||
| 内容記述 | application/pdf | |||||
| 形態 | ||||||
| 1147925 bytes | ||||||
| 著者版フラグ | ||||||
| 出版タイプ | VoR | |||||
| 日本十進分類法 | ||||||
| 主題 | 377.5 | |||||
| その他の言語のタイトル | ||||||
| その他のタイトル | 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 | |||||
| タイトル（ヨミ） | ||||||
| その他のタイトル | 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 | |||||
| 出版者 | ||||||
| 出版者 | 熊本大学 | |||||
| 資源タイプ | ||||||
| 内容記述 | 学位論文(Thesis) | |||||
| 資源タイプ・ローカル | ||||||
| 博士論文 | ||||||
| 資源タイプ・NII | ||||||
| Thesis or Dissertation | ||||||
| 資源タイプ・DCMI | ||||||
| text | ||||||
| 資源タイプ・ローカル表示コード | ||||||
| 03 | ||||||
| コメント | ||||||
| 熊本大学大学院医学教育部 臨床医科学専攻 | ||||||
| 学位番号 | ||||||
| 甲博医第1771号 | ||||||
