近日，瑞士苏黎世大学教授Christian Münz及其团队的研究显示，EBV诱导B细胞的中枢神经系统归巢，吸引炎性T细胞。相关论文于2025年8月6日发表在《自然》杂志上。

在这里，研究团队证明EBV扩增了人源化小鼠中神经系统的寡克隆T-bet⁺CXCR3⁺ B细胞。效应记忆CD8⁺ T细胞和CD4⁺ T_H1细胞以及CD4⁺ TH₁₇细胞共同迁移到ebv感染的人源化小鼠的大脑。T-bet⁺CXCR3⁺ B细胞可以在缺乏其他淋巴细胞的情况下定植脑膜下脑区并吸引T细胞。用利妥昔单抗消耗B细胞或阻断CXCR3可显著减少淋巴细胞向中枢神经系统的浸润。因此，该研究团队认为有症状的原发性EBV感染产生B细胞亚群，这些细胞亚群进入中枢神经系统，吸引T细胞，从而引发多发性硬化症。

据了解，流行病学资料表明，Epstein–Barr病毒（EBV）感染是多发性硬化症的主要环境危险因素，多发性硬化症是中枢神经系统（CNS）的主要自身免疫性疾病。然而，EBV感染如何引发多发性硬化症的发病机制尚不清楚。

附：英文原文

Title: EBV induces CNS homing of B cells attracting inflammatory T cells

Author: Lderach, Fabienne, Piteros, Ioannis, Fennell, anna, Bremer, Elena, Last, Mette, Schmid, Sandra, Rieble, Lisa, Campbell, Caroline, Ludwig-Portugall, Isis, Bornemann, Lea, Gruhl, Alexander, Eulitz, Klaus, Gueguen, Paul, Mietz, Juliane, Mller, Anne, Pezzino, Gaetana, Schmitz, Jrgen, Ferlazzo, Guido, Mautner, Josef, Mnz, Christian

Issue&Volume: 2025-08-06

Abstract: Epidemiological data have identified Epstein–Barr virus (EBV) infection as the main environmental risk factor for multiple sclerosis, the predominant autoimmune disease of the central nervous system (CNS)1. However, how EBV infection initiates multiple sclerosis pathogenesis remains unclear. Here we demonstrate that EBV expands oligoclonal T-bet+CXCR3+ B cells that home to the CNS in humanized mice. Effector memory CD8+ T cells and CD4+ TH1 cells as well as CD4+ TH17 cells co-migrate to the brain of EBV-infected humanized mice. T-bet+CXCR3+ B cells can colonize submeningeal brain regions in the absence of other lymphocytes and attract T cells. Depletion of B cells with rituximab or blocking of CXCR3 significantly decreases lymphocyte infiltration into the CNS. Thus, we suggest that symptomatic primary EBV infection generates B cell subsets that gain access to the CNS, attract T cells and thereby initiate multiple sclerosis.

DOI: 10.1038/s41586-025-09378-0

Source: https://www.nature.com/articles/s41586-025-09378-0