Bcl-3 is a member of the IκB protein family and an essential modulator of NF-κB activity. It is well established that Bcl-3 is critical for the normal development, survival and differentiation of adaptive immune cells, especially T cells. However, the regulation of immune cell function by Bcl-3 through metabolic pathways has rarely been studied. In this study, we explored the role of Bcl-3 in the metabolism and function of T cells via the mTOR pathway. We verified that the proliferation of Bcl-3-deficient Jurkat T cells was inhibited, but their activation was promoted, and Bcl-3 depletion regulated cellular energy metabolism by reducing intracellular ATP and ROS production levels and mitochondrial membrane potential. Bcl-3 also regulates cellular energy metabolism in naive CD4+ T cells. In addition, the knockout of Bcl-3 altered the expression of mTOR, Akt, and Raptor, which are metabolism-related genes, in Jurkat cells. This finding indicates that Bcl-3 may mediate the energy metabolism of T cells through the mTOR pathway, thereby affecting their function. Overall, we provide novel insights into the regulatory role of Bcl-3 in T-cell energy metabolism for the prevention and treatment of immune diseases.

中文翻译：

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Bcl-3通过能量代谢调节T细胞功能

Bcl-3 是 IκB 蛋白家族的成员，也是 NF-κB 活性的重要调节剂。众所周知，Bcl-3 对于适应性免疫细胞（尤其是 T 细胞）的正常发育、存活和分化至关重要。然而，Bcl-3通过代谢途径调节免疫细胞功能的研究却很少。在本研究中，我们通过 mTOR 途径探讨了 Bcl-3 在 T 细胞代谢和功能中的作用。我们验证了 Bcl-3 缺陷的 Jurkat T 细胞的增殖受到抑制，但其活化得到促进，并且 Bcl-3 耗竭通过降低细胞内 ATP 和 ROS 产生水平以及线粒体膜电位来调节细胞能量代谢。Bcl-3 还调节初始 CD4+ T 细胞的细胞能量代谢。此外，Bcl-3的敲除改变了Jurkat细胞中代谢相关基因mTOR、Akt和Raptor的表达。这一发现表明Bcl-3可能通过mTOR途径介导T细胞的能量代谢，从而影响其功能。总的来说，我们对 Bcl-3 在 T 细胞能量代谢中的调节作用提供了新的见解，以预防和治疗免疫疾病。