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Blood, 1 August 2001, Vol. 98, No. 3, pp. 743-753
IMMUNOBIOLOGY
Modulation of T-cell activation by the glucocorticoid-induced
leucine zipper factor via inhibition of nuclear factor
B
Emira Ayroldi,
Graziella Migliorati,
Stefano Bruscoli,
Cristina Marchetti,
Ornella Zollo,
Lorenza Cannarile,
Francesca D'Adamio, and
Carlo Riccardi
From the Department of Clinical and Experimental
Medicine, Section of Pharmacology, University of Perugia, Italy.
Previously a novel gene was identified that encodes a
glucocorticoid-induced leucine zipper (GILZ) whose expression is
up-regulated by dexamethasone. This study analyzed the role of GILZ in
the control of T-cell activation and its possible interaction with nuclear factor B (NF- B). Results indicate that GILZ inhibits both
T-cell receptor (TCR)-induced interleukin-2/interleukin-2 receptor
expression and NF- B activity. In particular, GILZ inhibits NF- B
nuclear translocation and DNA binding due to a direct
protein-to-protein interaction of GILZ with the NF- B subunits.
Moreover, GILZ-mediated modulation of TCR-induced responses is part of
a circuit because TCR triggering down-regulates GILZ expression. These
results identify a new molecular mechanism involved in the
dexamethasone-induced regulation of NF- B activity and T-cell activation.

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