颅骨通道的重塑调节神经炎症期间脑膜的免疫浸润，这一成果由马赛艾克斯大学Rejane Rua研究团队经过不懈努力而取得。相关论文发表在2025年12月29日出版的《免疫学》杂志上。

该研究团队发现骨通道在小鼠围产期形成，该研究团队开发了调节它们并评估它们对脑膜免疫的影响的方法。抗集落刺激因子1受体（αCSF1R）的骨髓细胞耗竭或核因子κ b配体抗受体激活剂（αRANKL）的靶向破骨细胞抑制减少了通道大小，而机械受体瞬时受体电位香兰素4 （TRPV4）驱动的骨重塑则扩大了通道大小。经通道操作后，淋巴细胞性脉络丛脑膜炎病毒（LCMV）感染αRANKL处理小鼠脑膜免疫浸润减少，TRPV4激活后浸润增加。在离体颅骨实验中，限制通道损害了颅骨来源的免疫细胞向脑膜的迁移，而增强重塑则促进了这一迁移。他们的发现揭示了骨重塑控制着头骨-脑膜轴，并强调了它在神经炎症期间免疫细胞迁移到脑膜中的作用。

据了解，脑膜位于颅骨和大脑之间，里面有监视大脑边界的免疫细胞。骨髓通过骨通道与脑膜通信，使免疫细胞运输，但对骨通道的形成和调节知之甚少。

附：英文原文

Title: Remodeling of skull bone channels regulates immune infiltration into the meninges during neuroinflammation

Author: Elisa Eme-Scolan, Michel Gomes, Alessandro Bani, Audrey Romano, Oussama Kassem, Annie Roussel-Queval, Baptiste Casel, Lotfi Slimani, Toby Lawrence, Rejane Rua

Issue&Volume: 2025-12-29

Abstract: The meninges, located between the skull and brain, harbor immune cells that monitor the brain borders. Skull marrow communicates with the meninges via bone channels, enabling immune-cell trafficking, but little is known about bone channel formation and modulation. We found that bone channels were formed during the perinatal stage in mice, and we developed approaches to modulate them and assess their impact on meningeal immunity. Myeloid cell depletion with anti-colony-stimulating factor 1 receptor (αCSF1R) or targeted osteoclast inhibition with anti-receptor activator of nuclear factor kappa-B ligand (αRANKL) reduced channel size, whereas mechanoreceptor transient receptor potential vanilloid 4 (TRPV4)-driven bone remodeling enlarged them. Following channel manipulation, lymphocytic choriomeningitis virus (LCMV) infection showed reduced meningeal immune infiltration in αRANKL-treated mice and increased infiltration with TRPV4 activation. In an ex vivo skull assay, restricting channels impaired skull-derived immune-cell migration to the meninges, whereas enhancing remodeling promoted it. Our findings reveal that bone remodeling controls the skull-to-meninges axis and highlight its role in immune-cell migration into the meninges during neuroinflammation.

DOI: 10.1016/j.immuni.2025.11.019

Source: https://www.cell.com/immunity/abstract/S1074-7613(25)00521-7