P2肽诱导的实验性变应性神经炎：一种研究轴突变性的模型。

P2-peptide induced experimental allergic neuritis: a model to study axonal degeneration.

作者信息

Hahn A F, Feasby T E, Wilkie L, Lovgren D

机构信息

Department of Clinical Neurological Sciences, University of Western Ontario, Victoria Hospital, London, Canada.

出版信息

Acta Neuropathol. 1991;82(1):60-5. doi: 10.1007/BF00310924.

DOI:10.1007/BF00310924

PMID:1719739

Abstract

In experimental allergic neuritis (EAN) severity of clinical disease and pathology correlate with the dose of antigen (Hahn et al., Lab Invest 59:115-125, 1988). To avoid axonal membrane contamination of the antigen, EAN was induced with a synthetic peptide, corresponding to residues 53-78 of bovine P2 myelin protein. Severity of EAN correlated with the dose of peptide in the inoculate. The relationship between demyelination, inflammation and axonal degeneration was studied. Low doses resulted in pure demyelination. Axonal degeneration occurred only with high doses of antigen and in association with very active mononuclear inflammation. The role of macrophages in producing axonal damage is discussed.

摘要

在实验性变应性神经炎（EAN）中，临床疾病的严重程度和病理学表现与抗原剂量相关（哈恩等人，《实验室研究》59:115 - 125，1988年）。为避免抗原的轴突膜污染，用一种合成肽诱导EAN，该合成肽对应牛P2髓磷脂蛋白的53 - 78位氨基酸残基。EAN的严重程度与接种物中肽的剂量相关。研究了脱髓鞘、炎症和轴突变性之间的关系。低剂量导致单纯脱髓鞘。轴突变性仅在高剂量抗原时出现，且与非常活跃的单核炎症相关。讨论了巨噬细胞在产生轴突损伤中的作用。