A new dexamethasone-induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death
A new dexamethasone-induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death
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DOI：
10.1016/s1074-7613(00)80398-2
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发表时间：
1997-12-01
期刊：
影响因子：
32.4
通讯作者：
Riccardi, C
中科院分区：
文献类型：
--
作者：
D'Adamio, F;Zollo, O;Riccardi, C
通过比较地塞米松（DEX）处理和未处理的小鼠胸腺细胞中表达的mRNA种类，我们已经确定了一个基因，糖皮质激素诱导的亮氨酸拉链（GILZ），编码亮氨酸拉链家族的一个新成员。发现GILZ在胸腺、脾和淋巴结的正常淋巴细胞中表达，而在其他非淋巴组织（包括脑、肾和肝）中检测到低表达或无表达。在胸腺细胞和外周T细胞中，GILZ基因表达由DEX诱导。此外，GILZ表达选择性地保护T细胞免于由抗CD3单克隆抗体处理诱导的凋亡，但不保护由其它凋亡刺激物处理诱导的凋亡。这种抗凋亡作用与Fas和Fas配体表达的抑制相关。因此，GILZ是参与调节T细胞凋亡的候选转录因子。
By comparing mRNA species expressed in dexamethasone (DEX)-treated and untreated murine thymocytes, we have identified a gene, glucocorticoid-induced leucine zipper (GILZ), encoding a new member of the leucine zipper family. GILZ was found expressed in normal lymphocytes from thymus, spleen, and lymph nodes, whereas low or no expression was detected in other nonlymphoid tissues, including brain, kidney, and liver. In thymocytes and peripheral T cells, GILZ gene expression is induced by DEX. Furthermore, GILZ expression selectively protects T cells from apoptosis induced by treatment with anti-CD3 monoclonal antibody but not by treatment with other apoptotic stimuli. This antiapoptotic effect correlates with inhibition of Fas and Fas ligand expression. Thus, GILZ is a candidate transcription factor involved in the regulation of apoptosis of T cells.