Department of Surgery, Child and Family Research Institute, The University of British Columbia Vancouver, BC, Canada.
Front Immunol. 2012 Aug 13;3:245. doi: 10.3389/fimmu.2012.00245. eCollection 2012.
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.
调节性 CD4(+) T 细胞与传统 CD4(+) T 细胞的相对活性最终维持着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（PI3K）及其下游正负调节因子的活性在控制不同效应 CD4(+) T 细胞亚群的免疫调节和激活之间的平衡方面起着主要作用。与需要激活 PI3K 以分化并介导其效应功能的效应 T 细胞不同，调节性 T 细胞依赖于该途径的最小激活来发育和维持其特征表型、功能和代谢状态。在这篇综述中，我们讨论了 PI3K 信号通路在 CD4(+) T 细胞分化和功能中的作用，并重点讨论了如何调节 T 细胞中的这条通路可以改变免疫反应的结果，最终使免疫耐受和炎症之间的平衡发生倾斜。
