The Role of the PI3K Signaling Pathway in CD4(+) T Cell Differentiation and Function.
The Role of the PI3K Signaling Pathway in CD4(+) T Cell Differentiation and Function.
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DOI：
10.3389/fimmu.2012.00245
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发表时间：
2012
影响因子：
7.3
通讯作者：
Levings MK
中科院分区：
文献类型：
--
作者：
Han JM;Patterson SJ;Levings MK
调节性与常规CD 4 + T细胞的相对活性最终维持了免疫耐受和炎症之间的微妙平衡。在分子水平上，磷脂酰肌醇3-激酶（PI 3 K）及其下游正和负调节因子的活性在控制免疫调节与效应CD 4 + T细胞的不同亚群的活化之间的平衡中具有主要作用。与需要活化PI 3 K以分化和介导其效应子功能的效应T细胞相反，调节性T细胞依赖于该途径的最小活化来发展和维持其特征性表型、功能和代谢状态。在这篇综述中，我们讨论了PI 3 K信号通路在CD 4 + T细胞分化和功能中的作用，并重点关注T细胞中该通路的调节如何改变免疫应答的结果，最终打破耐受和炎症之间的平衡。
The relative activity of regulatory versus conventional CD4+ T cells ultimately maintains the delicate balance between immune tolerance and inflammation. At the molecular level, the activity of phosphatidylinositol 3-kinase (PI3K) and its downstream positive and negative regulators has a major role in controlling the balance between immune regulation and activation of different subsets of effector CD4+ T cells. In contrast to effector T cells which require activation of the PI3K to differentiate and mediate their effector function, regulatory T cells rely on minimal activation of this pathway to develop and maintain their characteristic phenotype, function, and metabolic state. In this review, we discuss the role of the PI3K signaling pathway in CD4+ T cell differentiation and function, and focus on how modulation of this pathway in T cells can alter the outcome of an immune response, ultimately tipping the balance between tolerance and inflammation.
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