徳島大学 教育・研究者情報データベース(EDB)

1. (英) Maekawa Yoichi

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2. 石舟 智恵子([徳島大学.大学院医歯薬学研究部.医学域.先端医学教育研究プロジェクト]/[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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3. 九十九 伸一([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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4. (英) Hozumi Katsuto

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5. (英) Yagita Hideo

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6. 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) Notch controls the survival of memory CD4+ T cells by regulating glucose uptake.

(英) CD4+ T cells differentiate into memory T cells that protect the host from subsequent infection. In contrast, autoreactive memory CD4+ T cells harm the body by persisting in the tissues. The underlying pathways controlling the maintenance of memory CD4+ T cells remain undefined. We show here that memory CD4+ T cell survival is impaired in the absence of the Notch signaling protein known as recombination signal binding protein for immunoglobulin J region (Rbpj). Treatment of mice with a Notch inhibitor reduced memory CD4+ T cell numbers and prevented the recurrent induction of experimental autoimmune encephalomyelitis. Rbpj-deficient CD4+ memory T cells exhibit reduced glucose uptake due to impaired AKT phosphorylation, resulting in low Glut1 expression. Treating mice with pyruvic acid, which bypasses glucose uptake and supplies the metabolite downstream of glucose uptake, inhibited the decrease of autoimmune memory CD4+ T cells in the absence of Notch signaling, suggesting memory CD4+ T cell survival relies on glucose metabolism. Together, these data define a central role for Notch signaling in maintaining memory CD4+ T cells through the regulation of glucose uptake.

1. (英) Animals
2. (英) CD4-Positive T-Lymphocytes
3. (英) Glucose
4. (英) Glucose Transporter Type 1
5. (英) Humans
6. (英) Immunoglobulin J Recombination Signal Sequence-Binding Protein
7. (英) Mice
8. (英) Oncogene Protein v-akt
9. (英) Receptors, Antigen, T-Cell
10. (英) Receptors, Notch
11. (英) Signal Transduction

1. (英) Article.ELocationID: 10.1038/nm.3758

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

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