活化诱导细胞死亡（AICD）过程中FasL表达的调控。
The regulation of FasL expression during activation-induced cell death (AICD).
作者信息
Nguyen T, Russell J
机构信息
Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St Louis, MO, USA 63110.
出版信息
Immunology. 2001 Aug;103(4):426-34. doi: 10.1046/j.1365-2567.2001.01264.x.
Activation-induced cell death (AICD), a Fas ligand (FasL)-dependent pathway, is important for maintaining T-cell homeostasis. Interleukin-2 (IL-2), an enhancer of AICD, can also enhance FasL expression. However, we show that the level of FasL or FLIP protein did not correlate with the susceptibility to AICD. Some T cells expressed high levels of FasL yet failed to undergo AICD, while others expressed little FasL and were sensitive. AICD susceptibility did not correlate with the kinetics of FasL up-regulation or down-regulation. The down-regulation of FasL can be mediated by a metalloprotease. However, we describe an alternative mechanism for the loss of FasL by endocytosis. Endocytosis inhibitors such as cytochalasins, sodium azide, deoxyglucose, or low temperatures prevented the loss of FasL. KB8301, a metalloprotease inhibitor had no effect on the loss of FasL or AICD in the T cells. Enhancing FasL expression was not crucial for AICD and the down-regulation of FasL proceeded via endocytosis.
活化诱导的细胞死亡（AICD）是一种依赖Fas配体（FasL）的途径，对维持T细胞稳态很重要。白细胞介素-2（IL-2）是AICD的增强剂，也能增强FasL表达。然而，我们发现FasL或FLIP蛋白的水平与对AICD的敏感性无关。一些T细胞表达高水平的FasL但未能发生AICD，而另一些T细胞表达很少的FasL却很敏感。AICD敏感性与FasL上调或下调的动力学无关。FasL的下调可由金属蛋白酶介导。然而，我们描述了一种通过内吞作用导致FasL丢失的替代机制。诸如细胞松弛素、叠氮化钠、脱氧葡萄糖或低温等内吞作用抑制剂可阻止FasL的丢失。金属蛋白酶抑制剂KB8301对T细胞中FasL的丢失或AICD没有影响。增强FasL表达对AICD并不关键，且FasL的下调是通过内吞作用进行的。
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