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Blood, 1 February 2006, Vol. 107, No. 3, pp. 1039-1047.
Prepublished online as a Blood First Edition Paper on October 4, 2005; DOI 10.1182/blood-2005-05-2183.
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Submitted May 31, 2005
Accepted September 25, 2005
Increased GILZ expression in transgenic mice up-regulates TH-2 lymphokynes
Lorenza Cannarile, Francesca Fallarino, Massimiliano Agostini, Salvatore Cuzzocrea, Emanuela Mazzon, Carmine Vacca, Tiziana Genovese, Graziella Migliorati, Emira Ayroldi*, and Carlo Riccardi
Department of Clinical and Experimental Medicine, University of Perugia, Perugia, Italy
Department of Experimental Medicine, University of Perugia, Perugia, Italy
Department of Clinical and Experimental Medicine and Pharmacology, University of Messina, Messina, Italy
* Corresponding author; email: ayroldi{at}unipg.it.
GILZ (Glucocorticoid-induced leucine zipper), a gene induced by dexamethasone, is involved in control of T lymphocyte activation and apoptosis. In the present study, using GILZ transgenic mice (TG), which over-express GILZ in the T cell lineage, we demonstrate GILZ is implicated in T helper-2 (Th-2) response development. After in vitro stimulation by CD3/CD28 antibodies, peripheral naive CD4+ T cells from TG mice secrete more Th-2 cytokines such as interleukin (IL)-4 (IL-4), IL-5, IL-13, IL-10 and produce less T-helper-1 (Th-1) cytokines such as interferon-g (IFN- ) than wild-type mice (WT). CD4+ TG lymphocytes up-regulated Th-2 cytokine expression in the specific response to Ovalbumin chicken egg (OVA) antigen immunization. Up-regulation correlated with increased expression of GATA-3 and signal transducer and activator of transcription 6 (Stat6), Th-2-specific transcription factors and decreased expression of T-bet, a transcription factor involved in Th-1 differentiation. Finally, in TG mice delayed-type hypersensitivity, a Th-1 response, was inhibited and bleomycin-induced pulmonary fibrosis, a Th-2 mediated disease, was more severe.
These results indicate GILZ contributes to CD4+ commitment toward a Th-2 phenotype and suggest this contribution may be another mechanism accounting for glucocorticoid immunomodulation.
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