Morphologic study on experimental allergic neuritis mediated by T cell line specific for bovine P2 protein in Lewis rats.
Morphologic study on experimental allergic neuritis mediated by T cell line specific for bovine P2 protein in Lewis rats.
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发表时间：
1985-08
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通讯作者：
S. Izumo;C. Linington;H. Wekerle;R. Meyermann
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作者：
S. Izumo;C. Linington;H. Wekerle;R. Meyermann
对静脉注射牛P2蛋白特异性T细胞诱导的Lewis大鼠实验性变态反应性神经炎(EAN)进行了光镜和电子显微镜观察。组织学改变几乎完全局限于周围神经系统，最严重的是坐骨神经和腰骶神经根，而臂神经和颈神经根受累较小。病变包括水肿、细胞浸润、脱髓鞘，以及随后的轴突变性。可见浸润性巨噬细胞活跃地剥离髓鞘，受影响神经纤维的雪旺细胞质被推到周围，没有明显的变性迹象。病理改变的第一个证据是在接种后4天坐骨神经严重水肿。免疫组织化学显示白蛋白和纤维蛋白原存在于神经内膜间隙。在这些水肿性神经病变中可见肥大细胞脱颗粒。形成血管周围袖带的细胞浸润物不仅由单个核细胞组成，而且由许多粒细胞组成。在中枢神经系统中，脊髓内也可见脑膜细胞浸润，接种后7d，后柱也出现变性。后一种情况被认为是由于腰椎后根轴突受损所致的退行性变。在T细胞介导的EAN模型中，这些病理结果基本上与以前在常规诱导的EAN或人类格林-巴利综合征中报道的相同。因此，针对牛P2蛋白的T细胞可以在Lewis大鼠中诱导典型的EAN病变。对EAN这种转移模型的进一步研究将使我们能够阐明EAN和格林-巴利综合征的发病机制。
Light and electron microscope studies were performed on experimental allergic neuritis (EAN) passively induced in Lewis rats by the intravenous injection of T line cells specific for bovine P2 protein. Histologic changes were almost entirely restricted to the peripheral nervous system, being most severe in the sciatic nerve and lumbosacral nerve roots, whereas the brachial nerve and cervical nerve roots were involved to a lesser extent. The lesions were composed of edema, cellular infiltrates, demyelination, and, subsequently, axonal degeneration. Infiltrated macrophages were observed actively stripping the myelin, and the Schwann cell cytoplasm of affected nerve fibers was pushed to the periphery without distinct evidence of degeneration. The first evidence of pathologic change was severe edema in the sciatic nerve 4 days postinoculation. This edema was demonstrated immunohistochemically by the presence of albumin and fibrinogen in the endoneurial space. Mast cell degranulation was observed in these edematous nerve lesions. The cellular infiltrates which formed perivascular cuffs were composed of not only mononuclear cells but also many granulocytes. In the central nervous system, meningeal cell infiltration was also observed in the spinal cord, and after 7 days postinoculation degeneration of the posterior column was also found. This latter observation is thought to represent degeneration due to axonal damage of lumbosacral posterior roots. These pathologic findings in a T cell-mediated model of EAN were essentially the same as those previously reported in conventionally induced EAN or human Guillain-Barré Syndrome. Thus, T cells specific for bovine P2 protein can induce typical EAN lesions in the Lewis rat. The further investigation of this transfer model of EAN will enable us to clarify the pathogenesis of EAN and Guillain-Barré syndrome.