There is increasing interest in how immune cells, including those within the meninges at the blood-brain interface, influence brain function and mood disorders, but little data on humoral immunity in this context. Here, we show that in mice exposed to psychosocial stress, there is increased splenic B cell activation and secretion of the immunoregulatory cytokine interleukin (IL)-10. Meningeal B cells were prevalent in homeostasis but substantially decreased following stress, whereas Ly6C^hi monocytes increased, and meningeal myeloid cells showed augmented expression of activation markers. Single-cell RNA sequencing of meningeal B cells demonstrated the induction of innate immune transcriptional programmes following stress, including genes encoding antimicrobial peptides that are known to alter myeloid cell activation. Cd19^-/- mice, that have reduced B cells, showed baseline meningeal myeloid cell activation and decreased exploratory behaviour. Together, these data suggest that B cells may influence behaviour by regulating meningeal myeloid cell activation.

人们越来越关注免疫细胞（包括血脑界面脑膜内的免疫细胞）如何影响大脑功能和情绪障碍，但在这种情况下关于体液免疫的数据很少。在这里，我们发现在暴露于社会心理压力的小鼠中，脾 B 细胞活化和免疫调节细胞因子白细胞介素 (IL)-10 的分泌增加。脑膜 B 细胞在稳态中普遍存在，但在应激后显着减少，而 Ly6C ^hi单核细胞增加，脑膜髓细胞显示激活标志物的表达增加。脑膜 B 细胞的单细胞 RNA 测序证明了应激后先天免疫转录程序的诱导，包括编码已知会改变骨髓细胞活化的抗菌肽的基因。B 细胞减少的Cd19 ^{-/-小鼠表现出基线脑膜骨髓细胞活化和探索行为减少。}总之，这些数据表明 B 细胞可能通过调节脑膜髓细胞活化来影响行为。