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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >CD27 mediates interieukin-2-independent clonal expansion of the CD8(+) T cell without effector differentiation
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CD27 mediates interieukin-2-independent clonal expansion of the CD8(+) T cell without effector differentiation

机译：CD27介导不依赖效应子分化的CD8（+）T细胞interieukin-2独立克隆扩展

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摘要

The clonal expansion of antigen-specific CD8(+) T cells in response to microbial infections is essential for adaptive immunity. Although IL-2 has been considered to be primarily responsible for this process, quantitatively normal expansion occurs in the absence of IL-2 receptor signaling. Here, we show that ligating CD27 on CD8(+) T cells that have been stimulated through the T cell receptor causes their expansion in the absence of IL-2 by mediating two distinct cellular processes: enhancing cell cycling and promoting cell survival by maintaining the expression of IL-7 receptor a. This pathway for clonal expansion of the CD8(+) T cell is not associated with the development of a capacity either for production of IFN-gamma or for cytotoxic T lymphocyte function and, therefore, is uncoupled from differentiation. Furthermore, ligating CD27 increases the threshold concentration at which IL-2 induces IFN-gamma-producing capability by the CD8(+) T cell, suggesting that CD27 signaling may suppress effector differentiation. Finally, CD8(+) T cells that have been stimulated by the TCR/CD27 pathway maintain their capacity for subsequent expansion and effector differentiation in response to a viral challenge in vivo. Thus, the TCR/CD27 pathway enables the CD8(+) T cell to replicate by a process of self-renewal, which may contribute to the continuous generation of new effector CD8(+) T cells in persistent viral infections.
机译：抗原特异性CD8（+）T细胞对微生物感染的克隆扩增对于适应性免疫至关重要。尽管人们认为IL-2对此过程起主要作用，但在没有IL-2受体信号转导的情况下，定量的正常扩增发生了。在这里，我们显示，通过介导两个不同的细胞过程，将CD27连接到已通过T细胞受体刺激的CD8（+）T细胞上，导致它们在没有IL-2的情况下膨胀：通过维持细胞周期来增强细胞周期并促进细胞存活IL-7受体的表达a。 CD8（+）T细胞的克隆扩增途径与产生IFN-γ或细胞毒性T淋巴细胞功能的能力发展无关，因此与分化无关。此外，连接CD27可提高IL-2诱导CD8（+）T细胞诱导IFN-γ产生能力的阈值浓度，表明CD27信号传导可抑制效应子分化。最后，已被TCR / CD27途径刺激的CD8（+）T细胞在体内对病毒攻击的反应中保持了其随后的扩增和效应子分化的能力。因此，TCR / CD27途径使CD8（+）T细胞能够通过自我更新过程进行复制，这可能有助于在持续性病毒感染中连续产生新的效应CD8（+）T细胞。

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