Zou L P, Ma D H, Levi M, Wahren B, Wei L, Mix E, van der Meide P H, Link H, Zhu J
Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.
J Neuroimmunol. 1999 Feb 1;94(1-2):109-21. doi: 10.1016/s0165-5728(98)00232-x.
Experimental autoimmune neuritis (EAN) is an autoimmune inflammatory demyelinating disease of the peripheral nervous system (PNS), and represents an animal model of the human Guillain-Barré syndrome (GBS). In this study, we report that nasal administration of the neuritogenic peptide 180-199 and of the cryptic peptide 56-71 of the rat neuritogenic P0 protein of peripheral nerve myelin prevents EAN and attenuates ongoing EAN. Both peptides effectively decreased the severity and shortened clinical EAN. Both a prophylactic and a therapeutic approach proved to be beneficial. These effects were associated with T and B cells hyporesponsiveness to the peptide antigens, reflected by downregulated Th1 cell responses (interferon-gamma secretion) and macrophage function, whereas Th2 cell responses (IL-4 secretion) and transforming growth factor-beta mRNA expression were upregulated.
实验性自身免疫性神经炎(EAN)是一种外周神经系统(PNS)的自身免疫性炎性脱髓鞘疾病,是人类吉兰-巴雷综合征(GBS)的动物模型。在本研究中,我们报告经鼻给予外周神经髓鞘大鼠致神经炎P0蛋白的致神经炎肽180-199和隐蔽肽56-71可预防EAN并减轻正在发生的EAN。两种肽均有效降低了EAN的严重程度并缩短了临床病程。预防性和治疗性方法均被证明是有益的。这些作用与T和B细胞对肽抗原的低反应性有关,表现为Th1细胞反应(γ干扰素分泌)和巨噬细胞功能下调,而Th2细胞反应(IL-4分泌)和转化生长因子-β mRNA表达上调。