期刊
IMMUNITY
卷 30, 期 3, 页码 348-357出版社
CELL PRESS
DOI: 10.1016/j.immuni.2009.01.009
关键词
-
类别
资金
- Medical Research Council [G9722488, G9900061, MC_U137881016, G0500365] Funding Source: researchfish
- MRC [G9900061, G0500365, MC_U137881016, G9722488] Funding Source: UKRI
- Medical Research Council [G9722488, G0500365, G9900061, MC_U137881016] Funding Source: Medline
Environmental factors account for 75% of the risk of developing multiple sclerosis (MS). Numerous infections have been suspected as environmental disease triggers, but none of them has consistently been incriminated, and it is unclear how so many different infections may play a role. We show that a microbial peptide, common to several major classes of bacteria, can induce MS-like disease in humanized mice by crossreacting with a T cell receptor (TCR) that also recognizes a peptide from myelin basic protein, a candidate MS autoantigen. Structural analysis demonstrates this crossreactivity is due to structural mimicry of a binding hotspot shared by self and microbial antigens, rather than to degenerate TCR recognition. Biophysical studies reveal that the autoreactive TCR binding affinity is markedly lower for the microbial (mimicry) peptide than for the autoantigenic pepticle. Thus, these data suggest a possible explanation for the difficulty in incriminating individual infections in the development of MS.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据