B cells have been implicated in the pathogenesis of multiple sclerosis, but the mechanisms that guide B cell activation in the periphery and subsequent migration to the CNS remain incompletely understood. We previously showed that systemic inflammation induces an accumulation of B cells in the spleen in a CCR6/CCL20-dependent manner. In this study, we evaluated the role of CCR6/CCL20 in the context of myelin oligodendrocyte glycoprotein (MOG) protein–induced (B cell–dependent) experimental autoimmune encephalomyelitis (EAE). We found that CCR6 is upregulated on murine B cells that migrate into the CNS during neuroinflammation. In addition, human B cells that migrate across CNS endothelium in vitro were found to be CCR6⁺, and we detected CCL20 production by activated CNS-derived human endothelial cells as well as a systemic increase in CCL20 protein during EAE. Although mice that lack CCR6 expression specifically on B cells exhibited an altered germinal center reaction in response to MOG protein immunization, CCR6-deficient B cells did not exhibit any competitive disadvantage in their migration to the CNS during EAE, and the clinical and pathological presentation of EAE induced by MOG protein was unaffected. These data, to our knowledge, provide new information on the role of B cell–intrinsic CCR6 expression in a B cell–dependent model of neuroinflammation.

B 细胞与多发性硬化的发病机制有关，但指导 B 细胞在外周激活和随后迁移到中枢神经系统的机制仍未完全了解。我们之前表明全身炎症以 CCR6/CCL20 依赖性方式诱导脾脏中 B 细胞的积累。在本研究中，我们评估了 CCR6/CCL20 在髓鞘少突胶质细胞糖蛋白 (MOG) 蛋白诱导的（B 细胞依赖性）实验性自身免疫性脑脊髓炎 (EAE) 背景下的作用。我们发现 CCR6 在神经炎症期间迁移到中枢神经系统的鼠 B 细胞上上调。此外，在体外迁移穿过 CNS 内皮的人类 B 细胞被发现是 CCR6 ⁺，我们检测到活化的 CNS 衍生的人内皮细胞产生 CCL20，以及 EAE 期间 CCL20 蛋白的系统性增加。尽管在 B 细胞上缺乏 CCR6 特异性表达的小鼠表现出响应 MOG 蛋白免疫的生发中心反应改变，但 CCR6 缺陷的 B 细胞在 EAE 期间向 CNS 迁移并没有表现出任何竞争劣势，并且MOG蛋白诱导的EAE不受影响。据我们所知，这些数据提供了关于 B 细胞内在 CCR6 表达在 B 细胞依赖性神经炎症模型中的作用的新信息。