A new dexamethasone-induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death

被引：389

作者：

D'Adamio, F ^{[1
]}

Zollo, O ^{[1
]}

Moraca, R ^{[1
]}

Ayroldi, E ^{[1
]}

Bruscoli, S ^{[1
]}

Bartoli, A ^{[1
]}

Cannarile, L ^{[1
]}

Migliorati, G ^{[1
]}

Riccardi, C ^{[1
]}

机构：

[1] Univ Perugia, Dept Clin Med Pathol & Pharmacol, Pharmacol Sect, I-06100 Perugia, Italy

来源：

IMMUNITY | 1997年 / 7卷 / 06期

关键词：

D O I：

10.1016/S1074-7613(00)80398-2

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：803 / 812

页数：10

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