Colpitts Sara L, Kasper Lloyd H
Department of Microbiology and Immunology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755
Department of Microbiology and Immunology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755.
J Immunol. 2017 Jan 15;198(2):596-604. doi: 10.4049/jimmunol.1601438.
Autoimmune disorders of the CNS have complex pathogeneses that are not well understood. In multiple sclerosis and neuromyelitis optica spectrum disorders, T cells destroy CNS tissue, resulting in severe disabilities. Mounting evidence suggests that reducing inflammation in the CNS may start with modulation of the gut microbiome. The lymphoid tissues of the gut are specialized for the induction of regulatory cells, which are directly responsible for the suppression of CNS-damaging autoreactive T cells. Whether cause or effect, the onset of dysbiosis in the gut of patients with multiple sclerosis and neuromyelitis optica provides evidence of communication along the gut-brain axis. Thus, current and future therapeutic interventions directed at microbiome modulation are of considerable appeal.
中枢神经系统的自身免疫性疾病具有复杂的发病机制，目前尚未完全明确。在多发性硬化症和视神经脊髓炎谱系障碍中，T细胞会破坏中枢神经系统组织，导致严重残疾。越来越多的证据表明，减轻中枢神经系统的炎症可能始于对肠道微生物群的调节。肠道的淋巴组织专门用于诱导调节性细胞，这些细胞直接负责抑制损害中枢神经系统的自身反应性T细胞。无论因果关系如何，多发性硬化症和视神经脊髓炎患者肠道内的微生物群失调都为肠脑轴之间的交流提供了证据。因此，目前和未来针对微生物群调节的治疗干预措施具有相当大的吸引力。
