| ○種別 (必須): | □ | 学術論文 (審査論文)
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| ○言語 (必須): | □ | 英語
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| ○招待 (推奨): |
| ○審査 (推奨): | □ | Peer Review
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| ○カテゴリ (推奨): |
| ○共著種別 (推奨): |
| ○学究種別 (推奨): |
| ○組織 (推奨): |
| ○著者 (必須): | 1. | (英) Hisaeda H (日) (読)
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| ○学籍番号 (推奨): |
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| 2. | (英) Hamano S (日) (読)
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| 3. | (英) Mitoma-Obata C (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 4. | (英) Tetsutani K (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
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| 5. | (英) Imai T (日) (読)
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| 6. | (英) Waldmann H (日) (読)
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| 7. | (英) Himeno K (日) (読)
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| 8. | 安友 康二 ([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.病理系.生体防御医学])
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| ○題名 (必須): | □ | (英) Resistance to GITR signaling in antigen specific CD4+CD25+ regulatory T cells during plasmodium yoelii infection. (日)
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| ○副題 (任意): |
| ○要約 (任意): | □ | (英) CD4+ T cells are the major effector T cells against blood-stage Plasmodium yoelii infection. On the other hand, the lethal strain of P. yoelii (PyL) has acquired an escape mechanism from host T cell immunity by activating CD4+CD25+ regulatory T cells (Treg). Although the activation of Treg during PyL infection precludes the clearance of PyL from mice, it remains unclear whether activation of Treg is attributable to a specific response against PyL infection. Thus, we examined here whether Treg proliferate in an antigen-dependent manner during PyL infection. We also investigated the effector and regulatory mechanisms of Treg. Infection with PyL increased the number of CD4+CD25+ T cells, in which expression of Foxp3 mRNA is up-regulated. The Treg that were transferred into mice infected with PyL, but not with a non-lethal strain of P. yoelii (PyNL), proliferated during the initial 5 days following infection. The Treg from PyL-infected mice showed strong suppression compared with those from naive or PyNL-infected mice, and could suppress T cell activation by recognizing PyL- but not PyNL-derived antigens. Furthermore, the suppressive function of Treg activated in PyL-infected but not in naive mice could not be inhibited by treatment with an anti-glucocorticoid-induced TNFR family-related protein (GITR) mAb. These findings indicate that PyL infection specifically activates Treg that are specific for PyL-derived antigens. The infection also induces resistance for Treg to GITR signaling, and this eventually contributes to the escape of parasites from host T cell immunity. (日)
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| ○キーワード (推奨): | 1. | (英) Animals (日) (読)
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| 2. | (英) Antibodies, Monoclonal (日) (読)
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| 3. | (英) Antibodies, Protozoan (日) (読)
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| 4. | (英) Female (日) (読)
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| 5. | (英) Glucocorticoid-Induced TNFR-Related Protein (日) (読)
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| 6. | (英) Immunity, Innate (日) (読)
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| 7. | (英) Malaria (日) (読)
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| 8. | (英) Mice (日) (読)
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| 9. | (英) Mice, Inbred C57BL (日) (読)
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| 10. | (英) Plasmodium yoelii (日) (読)
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| 11. | (英) Receptors, Nerve Growth Factor (日) (読)
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| 12. | (英) Receptors, Tumor Necrosis Factor (日) (読)
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| 13. | (英) Self Tolerance (日) (読)
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| 14. | (英) T-Lymphocytes, Regulatory (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | European Journal of Immunology (European Federation of Immunological Societies)
(pISSN: 0014-2980, eISSN: 1521-4141)
| ○ISSN (任意): | □ | 0014-2980
ISSN: 0014-2980
(pISSN: 0014-2980, eISSN: 1521-4141) Title: European journal of immunologyTitle(ISO): Eur J ImmunolSupplier: European Federation of Immunological SocietiesPublisher: Wiley (NLM Catalog)
(Wiley)
(Scopus)
(CrossRef)
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| ○巻 (必須): | □ | 35
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| ○号 (必須): | □ | 12
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| ○頁 (必須): | □ | 3516 3524
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2005年 12月 初日 (平成 17年 12月 初日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1002/eji.200526073 (→Scopusで検索)
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| ○PMID (任意): | □ | 16304635 (→Scopusで検索)
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| ○備考 (任意): | 1. | (英) Article.Affiliation: Department of Immunology & Parasitology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan. (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 3. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
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