据“中央社”报道，台湾“中央研究院”分子生物研究所赖明宗研究团队，利用实验小鼠首次发现免疫控制分子Deltex1的全新功能。
人体内有众多的免疫细胞，其中T淋巴细胞(即T细胞)主导细胞免疫反应，T细胞担任的是指挥官角色，快速辨识病毒并调度功能不同的免疫细胞，与病原对抗。有关T细胞如何被启动活化，研究相当多，但对于T细胞静默的分子机制，科学家了解很少。
赖明宗研究团队的研究清楚呈现Deltex1于人体免疫T细胞活化过程中，扮演多种机制的修饰作用，对免疫研究学界有基础性的重要解释功用，受到国际瞩目。
研究团队是以先前在果蝇所发现的Deltex1分子为研究对象，Deltex1在哺乳类的功能一直不清楚，研究团队发现，Deltex1在T细胞静默时会大量表现，用来抑制T细胞活化，如果将Deltex1转殖基因表现在小鼠上，则小鼠T细胞几乎无法活化。
研究团队也证实，如果将Deltex1基因从小鼠剔除，T细胞会高度活化，小鼠产生自体抗体，并出现多重器官发炎，也就是说，Deltex1是个全新了解T细胞是否即将启动的重要因子，并且Deltex1也是T细胞静默讯息网络重要的一个开关。
“中研院”表示，对于T细胞为何静默的深入了解，将有助未来医学界临床运用。如能引导T细胞进入静默状态，很可能可以预防器官移植排斥作用和治疗自体免疫疾病。反之，掌握住如何唤醒静默中的T细胞，将可以更有效对抗癌细胞或病原体感染。（生物谷Bioon.com）
生物谷推荐原始出处：
Immunity, 09 July 2009 doi:10.1016/j.immuni.2009.04.017
Deltex1 Is a Target of the Transcription Factor NFAT that Promotes T Cell Anergy
Huey-Wen Hsiao1,2,4,Wen-Hsien Liu2,4,Chen-Jhe Wang2,Yu-Hsun Lo2,Yung-Hsuan Wu1,2,Si-Tse Jiang2andMing-Zong Lai1,2,3,,
1 Graduate Institute of Microbiology and Immunology, National Yang-Ming University, Taipei 11221, Taiwan, ROC
2 Institute of Molecular Biology, Academia Sinica, Taipei 11529, Taiwan, ROC
3 Graduate Institute of Immunology, National Taiwan University, Taipei 10002, Taiwan, ROC
The molecular process underlying Tcell anergy is incompletely understood. Deltex1 (DTX1) is a Notch target with unknown physiological function. Here we show that Dtx1 was a transcription target of nuclear factor of activated Tcells (NFAT) and participated in Tcell anergy. DTX1 protein was upregulated during Tcell anergy, and transgenic expression of Dtx1 attenuated Tcell activation. DTX1 inhibited Tcell activation by both E3-dependent and E3-independent mechanisms. In addition, DTX1 suppressed Tcell activation in the absence of its Notch-binding domain. Importantly, DTX1 regulated the expression of two anergy-associated molecules, growth arrest and DNA-damage-inducible 45 (Gadd45) and Cbl-b. DTX1 interacted with early growth response 2 (Egr-2) for optimum expression of Cbl-b. Furthermore, deficiency of DTX1 augmented Tcell activation, conferred resistance to anergy induction, enhanced autoantibody generation, and increased inflammation. DTX1 therefore represents a component downstream of calcium-NFAT signaling that regulates Tcell anergy.
