Induction Mechanisms of Memory T Cells

记忆T细胞的诱导机制

• 批准号: 14570276
• 负责人: TOKUHISA Takeshi
• 金额: $ 2.56万
• 依托单位: Chiba University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2002
• 资助国家: 日本
• 起止时间: 2002 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14570276/
• 关键词: Memory T cells; Transcription factor; BCL6; Transgenic mice; Homeostatic proliferation; Central memory T cells; BAZF; CD8 T cells; CD8T細胞; 好酸球性アレルギー; IL-5; 転写抑制; エフェクター細胞

Naive T cells proliferate and differentiate into memory cells after antigenic stimulation or in a lymphopenic environment. We showed here transient increases in memory phenotype CD8^+ T cell numbers in the lymphopenic environment of spleens of very young mice. The magnitude of the increase correlated with Bcl-6 expression in the T cells. Bcl-6 controlled the generation and maintenance of antigen-specific memory phenotype CD8^+ T cells in the spleens of immunized mice. These data suggest that Bcl-6, which is also essential for memory B cell development in germinal centers, is a key molecule for the establishment not only of memory T cells but also of the peripheral T cell compartment in infancy.

初始 T 细胞在抗原刺激后或在淋巴细胞减少的环境中增殖并分化为记忆细胞。我们在这里展示了幼年小鼠脾脏淋巴细胞减少环境中记忆表型 CD8^+ T 细胞数量的短暂增加。增加的幅度与 T 细胞中 Bcl-6 的表达相关。 Bcl-6 控制免疫小鼠脾脏中抗原特异性记忆表型 CD8^+ T 细胞的生成和维持。这些数据表明，Bcl-6 对于生发中心的记忆 B 细胞发育也至关重要，它不仅是记忆 T 细胞建立的关键分子，也是婴儿期外周 T 细胞区室建立的关键分子。

项目成果

Toyama, H., et al.: "Memory B cells without somatic hypermutation are generateded from Bcl6-deficient B cells."Immunity. 17. 329-339 (2002)

Toyama, H. 等人：“没有体细胞超突变的记忆 B 细胞是由 Bcl6 缺陷的 B 细胞产生的。”免疫。

Sata, M., et al.: "Hematopoietic stem cells differentiate into vascular cells that participate in the pathogenesis of atherosclerosis."Nature Med.. 8. 403-409 (2002)

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Kawamura, K., 等人：“DNA 聚合酶 θ 优先在淋巴组织中表达，并在人类癌症中受到预先调节。”Int.J.Cancer. 109. 9-16 (2004)

Yoshida, T., et al.: "Activation of STAT3 by the Hepatitis C virus core protein leads to cellular transformation."J.Exp.Med.. 196. 641-653 (2002)

Yoshida, T., et al.：“丙型肝炎病毒核心蛋白激活 STAT3 导致细胞转化。”J.Exp.Med.. 196. 641-653 (2002)

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Tada, Y., 等人：“Fas 配体在促进树突状细胞获得抗原方面的新作用。”J.Immunol.. 169. 2241-2245 (2002)