Identification of a putative G protein-coupled receptor induced during activation-induced apoptosis of T cells
Identification of a putative G protein-coupled receptor induced during activation-induced apoptosis of T cells
复制标题
DOI：
10.1006/cimm.1996.0051
复制
发表时间：
1996-02-25
影响因子：
4.3
通讯作者：
Choi, YW
中科院分区：
文献类型：
--
作者：
Choi, JW;Lee, SY;Choi, YW
在发育过程中，自身反应的未成熟胸腺细胞在胸腺中被克隆删除，这是一种建立T细胞耐受性（负选择）的现象。已经表明，胸腺中自身反应性未成熟T细胞的缺失是由T细胞受体（TCR）接合后的细胞凋亡介导的。TCR介导的未成熟胸腺细胞凋亡需要一组新基因的表达。为了确定在TCR介导的未成熟胸腺细胞死亡过程中需要哪些基因，我们试图鉴定在TCR介导的细胞死亡过程中表达增加的基因。利用mRNA差异显示技术，我们已经确定了一个新的基因，TDAG 8，它编码一个假定的G蛋白偶联受体。TDAG 8的表达在通过抗TCR抗体或通过佛波醇12-肉豆蔻酸酯13-乙酸酯加离子霉素活化T细胞时被极大地诱导。用糖皮质激素处理T细胞也极大地诱导TDAG 8的表达。在小鼠中，TDAG 8主要在胸腺和脾脏中表达。TDAG 8的组织特异性表达和在由TCR或糖皮质激素介导的T细胞的细胞死亡期间其表达的诱导表明其可能在活化诱导的T细胞的细胞死亡或分化中起作用。(C)出版社：Academic Press，Inc.
During development, self-reactive immature thymocytes are clonally deleted in the thymus, a phenomenon which establishes T cell tolerance (negative selection). It has been shown that the deletion of self-reactive immature T cells in the thymus is mediated by apoptosis upon T cell receptor (TCR) engagement. Apoptosis of immature thymocytes mediated by the TCR requires the expression of a new set of genes. To define which genes are required during the TCR-mediated death of immature thymocytes, we sought to identify genes whose expression is increased during TCR-mediated cell death. Using the technique of differential mRNA display, we have identified a novel gene, TDAG8, which encodes a putative G protein-coupled receptor. The expression of TDAG8 is greatly induced upon activation of T cells by anti-TCR antibody or by phorbol 12-myristate 13-acetate plus ionomycin. The treatment of T cells with glucocorticoids also greatly induces the expression of TDAG8. In mice, TDAG8 is predominantly expressed in thymus and spleen. The tissue-specific expression of TDAG8 and the induction of its expression during cell death of T cells mediated by the TCR or glucocorticoids suggest that it may have a role in activation-induced cell death or differentiation of T cells. (C) 1996 Academic Press, Inc.