Center for Brain and Spinal Cord Repair, Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University Medical Center, 460 West 12th Avenue, Columbus, OH 43210-1239, USA.
J Clin Invest. 2009 Oct;119(10):2990-9. doi: 10.1172/JCI39780. Epub 2009 Sep 21.
Traumatic injury to the mammalian spinal cord activates B cells, which culminates in the synthesis of autoantibodies. The functional significance of this immune response is unclear. Here, we show that locomotor recovery was improved and lesion pathology was reduced after spinal cord injury (SCI) in mice lacking B cells. After SCI, antibody-secreting B cells and Igs were present in the cerebrospinal fluid and/or injured spinal cord of WT mice but not mice lacking B cells. In mice with normal B cell function, large deposits of antibody and complement component 1q (C1q) accumulated at sites of axon pathology and demyelination. Antibodies produced after SCI caused pathology, in part by activating intraspinal complement and cells bearing Fc receptors. These data indicate that B cells, through the production of antibodies, affect pathology in SCI. One or more components of this pathologic immune response could be considered as novel therapeutic targets for minimizing tissue injury and/or promoting repair after SCI.
哺乳动物脊髓创伤会激活 B 细胞，导致自身抗体的合成。这种免疫反应的功能意义尚不清楚。本文作者表明，在缺乏 B 细胞的小鼠中，脊髓损伤 (SCI) 后的运动功能恢复得到改善，损伤病理学得到减轻。在 SCI 后，抗体分泌 B 细胞和 Igs 存在于 WT 小鼠的脑脊液和/或损伤的脊髓中，但在缺乏 B 细胞的小鼠中不存在。在具有正常 B 细胞功能的小鼠中，大量的抗体和补体成分 1q（C1q）在轴突病变和脱髓鞘部位积聚。SCI 后产生的抗体引起病理学改变，部分原因是激活了脊髓内补体和 Fc 受体阳性细胞。这些数据表明，B 细胞通过产生抗体影响 SCI 中的病理学。这种病理性免疫反应的一个或多个成分可以被视为新的治疗靶点，以最小化 SCI 后的组织损伤和/或促进修复。
