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5. Inhibited cell death, NF-kappaB activity and increased IL-10 in TCR-triggered thymocytes of transgenic mice overexpressing the glucocorticoid-induced protein GILZ.

Author

Delfino DV, Agostini M, Spinicelli S, Vacca C, and Riccardi C

Subjects
Animals, Antibodies, Monoclonal administration & dosage, CD3 Complex immunology, Cell Death immunology, Cytokines biosynthesis, Cytokines immunology, Mice, Mice, Transgenic, NF-kappa B immunology, Receptors, Antigen, T-Cell immunology, T-Lymphocytes cytology, T-Lymphocytes immunology, Thymus Gland immunology, Transcription Factors biosynthesis, Transcription Factors genetics, Apoptosis, Interleukin-10 biosynthesis, NF-kappa B antagonists & inhibitors, T-Lymphocytes metabolism, Thymus Gland cytology, Transcription Factors metabolism
Abstract

Glucocorticoids promote thymocyte apoptosis and modulate transcription of several genes including GILZ, which is strongly up-regulated in the thymus. We used transgenic mice overexpressing GILZ in the T-cell lineage to investigate TCR-triggered functions of GILZ-overexpressing thymocytes. TCR-triggered apoptosis, but not glucocorticoid-induced apoptosis, was inhibited in transgenic mice compared to their controls. In vivo anti-CD3 administration did not reduce CD4(+)CD8(+) thymocyte number. Analysis of TCR-triggered molecular changes indicated that p65 NF-kappaB nuclear translocation and DNA binding activity was inhibited in transgenic mice, which might be linked with apoptosis inhibition. IL-10 release increased whereas release of IL-2, IFN-gamma, IL-13 and IL-4 remained unchanged. These results support the hypothesis that GILZ regulates, at least in part, T-cell development by influencing thymus function at cellular and molecular levels.

Published
2006
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