Comparative histology of experimental allergic neuritis induced with minimum length neuritogenic peptides by adoptive transfer with sensitized cells or direct sensitization.
Comparative histology of experimental allergic neuritis induced with minimum length neuritogenic peptides by adoptive transfer with sensitized cells or direct sensitization.
复制标题
通过致敏细胞过继转移或直接致敏，用最小长度致神经源性肽诱导的实验性过敏性神经炎的比较组织学。
DOI：
10.1097/00005072-199109000-00010
复制
发表时间：
1991
影响因子：
3.2
通讯作者：
Mizisin,AP
中科院分区：
文献类型：
--
作者：
Powell,HC;Olee,T;Brostoff,SW;Mizisin,AP
使用代表牛髓磷脂蛋白P2的特定区域的合成肽，成功产生实验性变态反应性神经炎（EAN）所必需的T细胞表位的最小肽长度要求已显示涉及P2蛋白的残基61-70。在这项研究中，形态计量学分析被用来比较疾病后的刘易斯大鼠坐骨神经的组织学变化后，由P2特异性神经突原性T细胞系（P23），或者，直接接种合成肽代表残基60-70或61-70的P2蛋白序列。用残基61-70刺激的细胞系P23接种未能引起坐骨神经脱髓鞘。然而，用残余物60-70刺激的细胞在7天内产生炎症、神经内膜水肿、轻度脱髓鞘和轴突变性。相比之下，通过直接致敏用任一肽诱导的疾病更严重。形态测定分析显示，在对十肽致敏的动物中，炎症最严重。在坐骨神经中，轴突变性的频率与炎症程度成比例。脊髓根部的炎症尤其严重，包括无髓纤维在内的轴突受到广泛破坏。脊髓根改变与脊髓后白色束的沃勒变性相关，并且明显继发于神经内膜炎症。观察到血神经屏障（BNB）破坏，表现为与严重血管周围炎症相关的内皮细胞物理分离。
Using synthetic peptides representing specific regions of the bovine myelin protein P2, the minimum peptide length requirement for the T-cell epitope necessary for successful production of experimental allergic neuritis (EAN) has been shown to involve residues 61–70 of the P2protein. In this study, morphometric analysis was used to compare the histologic changes in sciatic nerves of Lewis rats after disease was induced by P2specific neuritogenic T-cell lines (P23) or, alternatively, by direct inoculation of synthetic peptides representing residues 60–70 or 61–70 of the P2protein sequence. Inoculation with cell line P23 stimulated with residue 61–70 failed to elicit demyelination in sciatic nerves. However, cells stimulated with residue 60–70 produced inflammation, endoneurial edema, mild demyelination and axonal degeneration within seven days. In contrast, disease induced with either peptide by direct sensitization was more severe. Morphometric analysis revealed that inflammation was most severe in animals sensitized to the decapeptide. In the sciatic nerve, axonal degeneration was proportional in frequency to the extent of inflammation. Inflammation was especially intense in spinal roots with extensive destruction of axons including unmyelinated fibers. Spinal root changes were associated with Wallerian degeneration in the posterior white matter tracts of the spinal cord and were apparently secondary to endoneurial inflammation. Disruption of the blood-nerve-barrier (BNB), evident as physical separation of endothelial cells in association with severe perivascular inflammation, was observed.