Müller-Durovic Bojana, Jäger Jessica, Bantug Glenn R, Hess Christoph
Center of Experimental Rheumatology, Department of Rheumatology, University Hospital and University of Zürich, Zürich, Switzerland.
Immunobiology Laboratory, Department of Biomedicine, University of Basel and University Hospital of Basel, Basel, Switzerland.
Trends Immunol. 2025 Jan;46(1):7-16. doi: 10.1016/j.it.2024.11.011. Epub 2024 Dec 20.
When B cells engage in an immune response, metabolic reprogramming is key to meeting cellular energetic and biosynthetic demands. Epstein-Barr virus (EBV) is a highly prevalent gamma-herpesvirus, latently infecting B cells for the human host's lifetime. By hijacking signaling pathways of T cell-dependent humoral immunity, EBV activates B cells in a T cell-independent manner, forcing lymphoblastoid transformation. Interlinked with this coercion of signaling pathways, EBV has also evolved strategies to manipulate B cell metabolism. In this opinion article we integrate recent findings from studies of B cell metabolic reprogramming after EBV infection and during antigen-specific activation, respectively. We hypothesize that defining EBV host-cell metabolic vulnerabilities that differ from pathways required for B cell immunity might uncover novel therapeutic targets against EBV-related diseases.
当B细胞参与免疫反应时，代谢重编程是满足细胞能量和生物合成需求的关键。爱泼斯坦-巴尔病毒（EBV）是一种高度流行的γ-疱疹病毒，可在人类宿主的一生中潜伏感染B细胞。通过劫持T细胞依赖性体液免疫的信号通路，EBV以T细胞非依赖性方式激活B细胞，促使淋巴母细胞转化。与这种信号通路的强制作用相关联，EBV还进化出了操纵B细胞代谢的策略。在这篇观点文章中，我们分别整合了EBV感染后和抗原特异性激活期间B细胞代谢重编程研究的最新发现。我们假设，确定与B细胞免疫所需途径不同的EBV宿主细胞代谢弱点，可能会揭示针对EBV相关疾病的新治疗靶点。
