BioTherapeutics Research Laboratory, Molecular Brain Research Group, Robarts Research Institute and Department of Microbiology and Immunology,The University of Western Ontario, 100 Perth Drive, London, Ontario, Canada.
J Clin Invest. 2009 Oct;119(10):2881-4. doi: 10.1172/JCI40839. Epub 2009 Sep 21.
The role of B cells and autoimmunity as contributing factors to poor neurological outcomes following spinal cord injury (SCI) is poorly understood. The study by Ankeny et al., in this issue of the JCI, identifies a new immunopathological mechanism arising after SCI in mice (see the related article beginning on page 2990). The study shows that B cells produce pathogenic antibodies that impair lesion repair, resulting in worse neurological outcome. This new understanding of SCI disease pathogenesis, if confirmed in humans, reveals potential avenues for the development of novel neuroprotective immunotherapies.
B 细胞和自身免疫在脊髓损伤 (SCI) 后神经功能不良结局中的作用尚未完全阐明。Ankeny 等人在本期《临床研究杂志》中的研究,在 SCI 后的小鼠模型中鉴定出一种新的免疫病理机制(见 2990 页相关文章)。该研究表明,B 细胞产生致病性抗体,损害损伤修复,导致更差的神经功能结局。如果在人类中得到证实,对 SCI 发病机制的这一新认识,揭示了开发新型神经保护免疫疗法的潜在途径。