徳島大学 教育・研究者情報データベース(EDB)

1. (英) Hisaeda H

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2. (英) Hamano S

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3. (英) Mitoma-Obata C

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4. (英) Tetsutani K

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5. (英) Imai T

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6. (英) Waldmann H

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7. (英) Himeno K

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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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(英) Resistance to GITR signaling in antigen specific CD4+CD25+ regulatory T cells during plasmodium yoelii infection.

(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.

1. (英) Animals
2. (英) Antibodies, Monoclonal
3. (英) Antibodies, Protozoan
4. (英) Female
5. (英) Glucocorticoid-Induced TNFR-Related Protein
6. (英) Immunity, Innate
7. (英) Malaria
8. (英) Mice
9. (英) Mice, Inbred C57BL
10. (英) Plasmodium yoelii
11. (英) Receptors, Nerve Growth Factor
12. (英) Receptors, Tumor Necrosis Factor
13. (英) Self Tolerance
14. (英) T-Lymphocytes, Regulatory

1. (英) Article.Affiliation: Department of Immunology & Parasitology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't