FAS LIGAND-INDUCED APOPTOSIS AS A MECHANISM OF IMMUNE PRIVILEGE
FAS LIGAND-INDUCED APOPTOSIS AS A MECHANISM OF IMMUNE PRIVILEGE
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DOI：
10.1126/science.270.5239.1189
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发表时间：
1995-11-17
期刊：
影响因子：
56.9
通讯作者：
FERGUSON, TA
中科院分区：
文献类型：
--
作者：
GRIFFITH, TS;BRUNNER, T;FERGUSON, TA
眼睛是一个特殊部位，无法耐受破坏性的炎症反应。因病毒感染而进入眼前房的炎症细胞发生了依赖于Fas（CD95） - Fas配体（FasL）的凋亡，且未造成组织损伤。相比之下，缺乏功能性Fas的gld小鼠在病毒感染时，发生炎症且眼部组织被侵袭，但没有细胞凋亡。当将Fas阳性而非Fas阴性的肿瘤细胞置于正常小鼠（而非Fas阴性小鼠）的离体眼前节内时，Fas阳性肿瘤细胞通过凋亡被杀死。在眼睛中可检测到Fas信使RNA和蛋白质。因此，Fas - FasL相互作用似乎是维持免疫赦免的一种重要机制。
The eye is a privileged site that cannot tolerate destructive inflammatory responses. inflammatory cells entering the anterior chamber of the eye in response to viral infection underwent apoptosis that was dependent on Fas (CD95)-Fas ligand (FasL) and produced no tissue damage. In contrast, viral infection in gld mice, which lack functional Fast, resulted in an inflammation and invasion of ocular tissue without apoptosis. Fas-positive but not Fas-negative tumor cells were killed by apoptosis when placed within isolated anterior segments of the eyes of normal but not Fast-negative mice. Fast messenger RNA and protein were detectable in the eye. Thus, Fas-FasL interactions appear to be:an important mechanism for the maintenance of immune privilege.