实验性自身免疫性脑脊髓炎
髓鞘少突胶质细胞糖蛋白
生物
多发性硬化
微生物学
罗伊乳杆菌
炎症
自身免疫性疾病
脑脊髓炎
免疫学
细菌
肠道菌群
微生物
益生菌
遗传学
抗体
作者
Eiji Miyauchi,Seok Won Kim,Wataru Suda,Masami Kawasumi,Satoshi Onawa,Naoko Taguchi‐Atarashi,Hidetoshi Morita,Todd D. Taylor,Masahira Hattori,Hiroshi Ohno
出处
期刊:Nature
[Springer Nature]
日期:2020-08-26
卷期号:585 (7823): 102-106
被引量:143
标识
DOI:10.1038/s41586-020-2634-9
摘要
Accumulating evidence indicates that gut microorganisms have a pathogenic role in autoimmune diseases, including in multiple sclerosis1. Studies of experimental autoimmune encephalomyelitis (an animal model of multiple sclerosis)2,3, as well as human studies4-6, have implicated gut microorganisms in the development or severity of multiple sclerosis. However, it remains unclear how gut microorganisms act on the inflammation of extra-intestinal tissues such as the spinal cord. Here we show that two distinct signals from gut microorganisms coordinately activate autoreactive T cells in the small intestine that respond specifically to myelin oligodendrocyte glycoprotein (MOG). After induction of experimental autoimmune encephalomyelitis in mice, MOG-specific CD4+ T cells are observed in the small intestine. Experiments using germ-free mice that were monocolonized with microorganisms from the small intestine demonstrated that a newly isolated strain in the family Erysipelotrichaceae acts similarly to an adjuvant to enhance the responses of T helper 17 cells. Shotgun sequencing of the contents of the small intestine revealed a strain of Lactobacillus reuteri that possesses peptides that potentially mimic MOG. Mice that were co-colonized with these two strains showed experimental autoimmune encephalomyelitis symptoms that were more severe than those of germ-free or monocolonized mice. These data suggest that the synergistic effects that result from the presence of these microorganisms should be considered in the pathogenicity of multiple sclerosis, and that further study of these microorganisms may lead to preventive strategies for this disease.
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