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神经干/祖细胞表达共刺激分子,这些分子受到炎症和凋亡刺激的差异调节。

Neural stem/progenitor cells express costimulatory molecules that are differentially regulated by inflammatory and apoptotic stimuli.

作者信息

Imitola Jaime, Comabella Manuel, Chandraker Anil K, Dangond Fernando, Sayegh Mohamed H, Snyder Evan Y, Khoury Samia J

机构信息

Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.

出版信息

Am J Pathol. 2004 May;164(5):1615-25. doi: 10.1016/S0002-9440(10)63720-0.

Abstract

Increased expression of the costimulatory molecule CD80 (B7-1) was noted in the subventricular zone of the brain during the course of experimental autoimmune encephalomyelitis (EAE). This area of the brain is a neural stem cell (NSC) niche in the adult. We show that isolated NSCs from adult brain express CD80 and CD86 (B7-2) and this expression is increased after exposure to IFN-gamma or TNF-alpha, the prototypical Th1 cytokines expressed during EAE. CD80 and CD86 expressed by NSCs are functional and can costimulate allogeneic cells in a mixed lymphocyte reaction. Furthermore, cross-linking of CD80 on the surface of NSCs results in apoptosis of NSCs. In vitro, we show that T cells can interact with NSCs and form conjugates with redistribution of CD3 on the surface of T cells to the area of contact. These data raise the possibility that during CNS inflammatory diseases such as EAE, NSCs may express immune molecules and interact with the inflammatory environment potentially resulting in injury to the NSCs, which may have implications for repair mechanisms in the central nervous system.

摘要

在实验性自身免疫性脑脊髓炎(EAE)病程中,发现共刺激分子CD80(B7-1)在脑室内下区的表达增加。该脑区是成体中的神经干细胞(NSC)龛。我们发现,从成体脑中分离的NSC表达CD80和CD86(B7-2),并且在暴露于EAE期间表达的典型Th1细胞因子IFN-γ或TNF-α后,这种表达会增加。NSC表达的CD80和CD86具有功能,并且可以在混合淋巴细胞反应中共刺激异基因细胞。此外,NSC表面CD80的交联导致NSC凋亡。在体外,我们发现T细胞可以与NSC相互作用并形成结合物,T细胞表面的CD3重新分布至接触区域。这些数据提示,在诸如EAE的中枢神经系统炎性疾病期间,NSC可能表达免疫分子并与炎性环境相互作用,这可能会导致NSC损伤,这可能对中枢神经系统的修复机制有影响。

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