实验性自身免疫性脑脊髓炎
生物
多发性硬化
免疫学
自身免疫性疾病
自身免疫
脑脊髓炎
神经科学
医学
免疫系统
抗体
作者
Naresha Saligrama,Fan Zhao,Michael J. Sikora,William S. Serratelli,Ricardo A. Fernandes,David M. Louis,Winnie Yao,Xuhuai Ji,Juliana Idoyaga,Vinit B. Mahajan,Lars M. Steinmetz,Yueh-hsiu Chien,Stephen L. Hauser,Jorge R. Oksenberg,K. Christopher García,Mark M. Davis
出处
期刊:Nature
[Nature Portfolio]
日期:2019-08-07
卷期号:572 (7770): 481-487
被引量:192
标识
DOI:10.1038/s41586-019-1467-x
摘要
Experimental autoimmune encephalomyelitis is a model for multiple sclerosis. Here we show that induction generates successive waves of clonally expanded CD4+, CD8+ and γδ+ T cells in the blood and central nervous system, similar to gluten-challenge studies of patients with coeliac disease. We also find major expansions of CD8+ T cells in patients with multiple sclerosis. In autoimmune encephalomyelitis, we find that most expanded CD4+ T cells are specific for the inducing myelin peptide MOG35–55. By contrast, surrogate peptides derived from a yeast peptide major histocompatibility complex library of some of the clonally expanded CD8+ T cells inhibit disease by suppressing the proliferation of MOG-specific CD4+ T cells. These results suggest that the induction of autoreactive CD4+ T cells triggers an opposing mobilization of regulatory CD8+ T cells. Activated clonally expanded CD4+ T cells display specificity to the myelin peptide MOG, whereas clonally expanded CD8+ T cells depend on T cell receptor recognition of unrelated surrogate peptides and have a regulatory function.
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