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J Biol Chem, Vol. 274, Issue 5, 3222-3227, January 29, 1999
From the Laboratory of Immune Cell Biology, NCI, National
Institutes of Health, Bethesda, Maryland 20892-1152
We previously identified a Fas ligand regulatory
element (FLRE) in the Fas ligand (fasL) promoter that binds
Egr family proteins and demonstrated that Egr-3 (PILOT) but not Egr-1
(NGFI-A, Krox-24, Tis-8, and Zif-268) induces transcription of
fasL. The aberrant CD4
Role of Egr-2 in Up-regulation of Fas Ligand in Normal T Cells
and Aberrant Double-negative lpr and gld T
Cells
CD8 T
cells from lpr/lpr and gld/gld mice, which have
mutations in the genes encoding Fas and FasL, respectively, have an
activated phenotype and constitutively express high levels of
fasL mRNA, prompting us to ask what role if any the
FLRE and Egr family proteins have in this aberrant expression of
fasL. Unstimulated MRL-lpr/lpr and
C3H-gld/gld CD4CD8 T cells
constitutively contained high levels of two proteins that bound to the
FLRE. Supershift analysis revealed these proteins to be Egr-1 and Egr-2
(Krox-20); Egr-3 was not detected. Activation of normal lymph node
cells resulted in increased expression of Egr-1, -2, and -3. As with
egr-3, expression of egr-2 was blocked by
cyclosporin A. Although overexpressed Egr-1 was ineffective, overexpressed Egr-2 was as potent as Egr-3 in inducing fasL
promoter-dependent reporter constructs in T cell hybridomas
and HeLa cells, and both up-regulated endogenous fasL
mRNA in HeLa cells. FasL-dependent reporter constructs
in MRL-lpr/lpr and C3H-gld/gld
CD4CD8 T cells were constitutively active,
and this activity was largely prevented by mutation of the critical Egr
family binding element. Thus, Egr-2, in addition to Egr-3, regulates
FasL expression in activated normal T cells, and Egr-2 is likely to
play a direct role in aberrant fasL up-regulation in
lpr/lpr and gld/gld
CD4CD8 T cells.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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