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在实验性变应性神经炎(EAN)过程中,施万细胞会发生凋亡。

Schwann cell undergoes apoptosis during experimental allergic neuritis (EAN).

作者信息

Conti G, Scarpini E, Rostami A, Livraghi S, Baron P L, Pleasure D, Scarlato G

机构信息

Institute of Neurology, Dino Ferrari Center, University of Milan, IRCCS Ospedale Maggiore Policlinico, Italy.

出版信息

J Neurol Sci. 1998 Nov 26;161(1):29-35. doi: 10.1016/s0022-510x(98)00260-3.

Abstract

Schwann cell apoptosis is not detectable in the normal mature mammalian peripheral nervous system (PNS). However, during PNS cell-mediated demyelination, apoptosis contributes to the elimination of endoneurial T-lymphocytes. We report here that approximately 10% of Schwann cells die by apoptosis during the early phases of recovery from experimental autoimmune neuritis (EAN) in the adult rat, a model for the Guillain-Barrè syndrome. Schwann cell apoptosis, follows endoneurial T-cell clearance, and is prominent in the nerve roots, the site of most severe segmental demyelination, but is rare in the more distal regions of the PNS, where Wallerian degeneration predominates. Further immunological analysis showed that the p75 neurotrophin receptor (p75NTR) is expressed in 2% of both apoptotic and non apoptotic Schwann cells, while Ki-67, a marker of cell proliferation, is expressed in 20% of apoptotic and in 1% of non apoptotic Schwann cells. Our new observations indicate that apoptosis during cell-mediated demyelination can be a phenomenon related either to the development or the recovery of autoimmune cell mediated inflammation.

摘要

在正常成熟的哺乳动物外周神经系统(PNS)中,未检测到施万细胞凋亡。然而,在PNS细胞介导的脱髓鞘过程中,凋亡有助于消除神经内膜T淋巴细胞。我们在此报告,在成年大鼠实验性自身免疫性神经炎(EAN,格林-巴利综合征的一种模型)恢复的早期阶段,约10%的施万细胞通过凋亡死亡。施万细胞凋亡发生在神经内膜T细胞清除之后,在神经根中很明显,神经根是最严重节段性脱髓鞘的部位,但在PNS更远端区域则很少见,在这些区域沃勒变性占主导。进一步的免疫学分析表明,p75神经营养因子受体(p75NTR)在2%的凋亡和非凋亡施万细胞中表达,而细胞增殖标志物Ki-67在20%的凋亡施万细胞和1%的非凋亡施万细胞中表达。我们的新观察结果表明,细胞介导的脱髓鞘过程中的凋亡可能是一种与自身免疫细胞介导炎症的发展或恢复相关的现象。

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