T 细胞受体依赖性调节脂质筏控制 naïve CD8+ T 细胞动态平衡。
T cell receptor-dependent regulation of lipid rafts controls naive CD8+ T cell homeostasis.
机构信息
Immunology and Inflammation Program, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010, Australia.
出版信息
Immunity. 2010 Feb 26;32(2):214-26. doi: 10.1016/j.immuni.2009.11.014. Epub 2010 Feb 4.
T cell receptor (TCR) contact with self ligands keeps T cells alive and is shown here to cause naive CD8(+), but not CD4(+), T cells to be hypersensitive to certain gamma(c) cytokines, notably interleukin (IL)-2, IL-15, and IL-7. Hypersensitivity of CD8(+) T cells to IL-2 was dependent on a low-level TCR signal, associated with high expression of CD5 and GM1, a marker for lipid rafts, and was abolished by disruption of lipid rafts. By contrast, CD4(+) T cells expressed low amounts of GM1 and were unresponsive to IL-2. Physiologically, sensitivity to IL-7 and IL-15 maintains survival of resting CD8(+) T cells, whereas sensitivity to IL-2 may be irrelevant for normal homeostasis but crucial for the immune response. Thus, TCR contact with antigen upregulates GM1 and amplifies responsiveness of naive CD8(+) T cells to IL-2, thereby making the cells highly sensitive to exogenous IL-2 from CD4(+) T helper cells.
T 细胞受体 (TCR) 与自身配体的接触使 T 细胞存活，并导致这里显示的幼稚 CD8(+)，而不是 CD4(+)，T 细胞对某些 γ(c)细胞因子（特别是白细胞介素 (IL)-2、IL-15 和 IL-7）过度敏感。CD8(+) T 细胞对 IL-2 的高敏性依赖于低水平的 TCR 信号，与 CD5 和 GM1 的高表达相关，GM1 是脂筏的标志物，而脂筏的破坏则消除了高敏性。相比之下，CD4(+) T 细胞表达少量的 GM1，对 IL-2 无反应。从生理上讲，对 IL-7 和 IL-15 的敏感性维持了静止 CD8(+)T 细胞的存活，而对 IL-2 的敏感性可能与正常体内平衡无关，但对免疫反应至关重要。因此，TCR 与抗原的接触上调 GM1，并放大幼稚 CD8(+)T 细胞对 IL-2 的反应性，从而使细胞对来自 CD4(+)T 辅助细胞的外源性 IL-2 高度敏感。
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