PI3K/AKT signaling and systemic autoimmunity

PI3K/AKT signaling and systemic autoimmunity
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DOI:
10.1385/ir:31:1:47
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发表时间:
2005-01-01
影响因子:
4.4
通讯作者:
Mohan, C
Mohan, C
中科院分区:
医学4区
文献类型:
--
作者:
Patel, RK;Mohan, C

文献摘要

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磷酸肌醇 3-激酶 (PI3K)/Akt 信号轴在细胞增殖和生长信号传导中发挥重要作用。关于免疫系统,越来越多的数据正在帮助阐明该途径在淋巴细胞发育中的作用,并表明导致该途径激活不受调节的扰动如何可能产生系统性自身免疫或恶性肿瘤。已经描述了该信号通路关键介质的各种敲除和转基因小鼠模型。许多导致该途径激活的模型表现出系统性自身免疫的特征,将该途径与自身免疫性疾病联系起来。在这里,我们回顾了最近描述的表现出激活的 PI3K/Akt 信号传导的小鼠模型以及该途径在自身免疫性疾病中的潜在作用,并讨论了这些发现的治疗意义。
The phosphoinositide 3-kinase (PI3K)/Akt signaling axis plays an important role in cellular proliferation and growth signaling. With respect to the immune system, a growing body of data is helping to elucidate the role of this pathway in lymphocyte development, as well as to show how perturbations that lead to unregulated activation in this pathway may produce systemic autoimmunity or malignancy. Various knockout and transgenic murine models have been described for key mediators of this signaling pathway. Many of these models resulting in the activation of this pathway demonstrate features of systemic autoimmunity, linking this pathway to autoimmune disease. Here, we review recently described murine models that exhibit activated PI3K/Akt signaling and the potential role this pathway in autoimmune disease, and also discuss the therapeutic implications of these findings.