期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 6, 期 7, 页码 1126-1134出版社
ELSEVIER
DOI: 10.1016/j.intimp.2006.02.001
关键词
glucocorticoid; GILZ; thymocyte; T-cell receptor; cell death; NF-kappa B
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-kappa B 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. (c) 2006 Elsevier B.V All rights reserved.
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