Abstract：
The L-tryptophan (Trp) transport system is highly selective for Trp with affinity in the nanomolar range. This transport system is augmented in human interferon (IFN)-γ-treated and indoleamine 2,3-dioxygenase 1 (IDO1)-expressing cells. Up-regulated cellular uptake of Trp causes a reduction in extracellular Trp and initiates immune suppression. Recent studies demonstrate that both IDO1 and tryptophanyl-tRNA synthetase (TrpRS), whose expression levels are up-regulated by IFN-γ, play a pivotal role in high-affinity Trp uptake into human cells. Furthermore, overexpression of tryptophan 2,3-dioxygenase (TDO2) elicits a similar effect as IDO1 on TrpRS-mediated high-affinity Trp uptake. In this review, we summarize recent findings regarding this Trp uptake system and put forward a possible molecular mechanism based on Trp deficiency induced by IDO1 or TDO2 and tryptophanyl-AMP production by TrpRS.
摘要：
L-色氨酸（Trp）转运系统对Trp具有高度选择性，亲和力在纳摩尔范围内。在人干扰素（IFN）-γ处理的和吲哚胺2,3-双加氧酶1（IDO1）表达的细胞中，这种运输系统得到了增强。上调Trp的细胞摄取导致细胞外Trp减少并引发免疫抑制。最近的研究表明，IDO1和色氨酸-tRNA合成酶（TrpRS），其表达水平由IFN-γ上调，在人细胞的高亲和力Trp摄取中起关键作用。此外，色氨酸2,3-双加氧酶（TDO2）的过表达对TrpRS介导的高亲和力Trp摄取具有与IDO1相似的作用。在这次审查中,我们总结了有关Trp摄取系统的最新发现，并提出了基于IDO1或TDO2诱导的Trp缺乏和TrpRS产生色氨酸-AMP的可能分子机制。
