Ethell Douglas W, Buhler Lillian A
Division of Biomedical Sciences, University of California-Riverside, 900 University Avenue, Riverside, California 92521-0121, USA.
J Clin Immunol. 2003 Sep;23(5):363-70. doi: 10.1023/a:1025317516396.
While defective apoptosis predisposes to neoplasia, inappropriate apoptosis in the brain leads to permanent neurological deficits. Disregulated apoptosis has been implicated in several neurodegenerative disorders including Alzheimer's, Parkinson's, and Huntington's diseases. Recent reports have suggested that the key apoptosis regulator Fas ligand (FasL) may participate in both neuronal and immune cell apoptosis in Alzheimer's disease. FasL has also been implicated as a negative regulator for the inflammatory component of the demyelinating brain disorder multiple sclerosis (MS). Here, we discuss how FasL-mediated apoptosis may balance immune cell access to the brain with Alzheimer's disease and MS representing extremes of too little and too much immune access, respectively.
虽然凋亡缺陷易引发肿瘤形成,但大脑中不适当的凋亡会导致永久性神经功能缺损。凋亡失调与包括阿尔茨海默病、帕金森病和亨廷顿病在内的多种神经退行性疾病有关。最近的报告表明,关键的凋亡调节因子Fas配体(FasL)可能参与阿尔茨海默病中神经元和免疫细胞的凋亡。FasL也被认为是脱髓鞘性脑部疾病多发性硬化症(MS)炎症成分的负调节因子。在此,我们讨论FasL介导的凋亡如何在阿尔茨海默病和MS中分别平衡免疫细胞进入大脑的情况,阿尔茨海默病代表免疫进入过少的极端情况,而MS代表免疫进入过多的极端情况。