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

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 lym...

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Bibliographic Details
Published in:Immunity (Cambridge, Mass.) Mass.), 1997-12, Vol.7 (6), p.803-812
Main Authors: D'Adamio, F, Zollo, O, Moraca, R, Ayroldi, E, Bruscoli, S, Bartoli, A, Cannarile, L, Migliorati, G, Riccardi, C
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Animals
Apoptosis
Base Sequence
Cell Line
Dexamethasone - pharmacology
DNA, Complementary
Fas Ligand Protein
fas Receptor - biosynthesis
fas Receptor - immunology
Gene Expression
Leucine Zippers - genetics
Leucine Zippers - immunology
Membrane Glycoproteins - biosynthesis
Membrane Glycoproteins - immunology
Mice
Mice, Inbred C3H
Molecular Sequence Data
Receptor-CD3 Complex, Antigen, T-Cell - immunology
Subcellular Fractions
T-Lymphocytes - drug effects
T-Lymphocytes - immunology
T-Lymphocytes - radiation effects
Tissue Distribution
Transfection
Ultraviolet Rays
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Summary: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.
ISSN:1074-7613
DOI:10.1016/S1074-7613(00)80398-2