髓鞘少突胶质细胞糖蛋白的一个隐蔽表位对实验性自身免疫性脑脊髓炎的改善作用
Amelioration of EAE by a cryptic epitope of myelin oligodendrocyte glycoprotein.
作者信息
Lyons Jeri A, Riter Melissa M, Almatrook Alaa M, Ramsbottom Michael J, Cross Anne H
机构信息
Department of Biomedical Sciences, University of Wisconsin - Milwaukee, Milwaukee, WI 53211, USA; Department of Neurology and Neurosurgery, Washington University School of Medicine, Saint Louis, MO, USA 63110.
Department of Biomedical Sciences, University of Wisconsin - Milwaukee, Milwaukee, WI 53211, USA.
出版信息
J Neuroimmunol. 2016 Nov 15;300:66-73. doi: 10.1016/j.jneuroim.2016.06.006. Epub 2016 Jun 24.
Abstract
Previous work demonstrated that EAE induced by recombinant human MOG was B cell-dependent. Data presented here reveal a T cell response to MOG61-85 in human rMOG-immunized B cell mice not observed in WT mice. Further study revealed this peptide to be a cryptic epitope in WT mice. Co-immunization of B cell mice with MOG35-55 and MOG61-85 peptides led to less severe disease compared to mice immunized with MOG35-55 alone. Disease amelioration was associated with decreased production of Interferon-γ by lymph node cells. Thus, MOG61-85 represents a protective epitope to human rMOG induced EAE in B cell mice.
摘要
先前的研究表明，重组人髓鞘少突胶质细胞糖蛋白（MOG）诱导的实验性自身免疫性脑脊髓炎（EAE）依赖于B细胞。此处呈现的数据显示，在用人重组MOG免疫的B细胞小鼠中可观察到针对MOG61 - 85的T细胞反应，而在野生型（WT）小鼠中未观察到。进一步研究表明，该肽段在WT小鼠中是一个隐蔽表位。与单独用MOG35 - 55免疫的小鼠相比，用MOG35 - 55和MOG61 - 85肽段共同免疫B细胞小鼠导致的疾病症状较轻。疾病改善与淋巴结细胞产生的γ干扰素减少有关。因此，MOG61 - 85代表了在B细胞小鼠中对人重组MOG诱导的EAE具有保护作用的表位。
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