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J. Biol. Chem., Vol. 277, Issue 9, 6838-6845, March 1, 2002
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From the Peroxisome proliferator-activated receptors
(PPARs) are transcription factors that belong to the nuclear hormone
receptor superfamily. PPAR
Nuclear Receptor Peroxisome Proliferator-activated Receptor
(PPAR) Is Expressed in Resting Murine Lymphocytes
THE PPAR
IN T AND B LYMPHOCYTES IS BOTH
TRANSACTIVATION AND TRANSREPRESSION COMPETENT*
§,, and¶
Department of Pathology, University
of Utah School of Medicine, Salt Lake City, Utah 84132 and the
¶ Geriatric Research, Education, and Clinical Center, Veterans
Affairs Medical Center, Salt Lake City, Utah 84112
and PPAR
ligands have been
demonstrated to exert anti-inflammatory activities in macrophages by
repressing the activities of several transcription factors. PPAR is
expressed in T lymphocytes and may play a role in cytokine production,
cellular proliferation, and susceptibility to apoptosis. Herein, we
demonstrate that T and B lymphocytes constitutively express PPAR.
PPAR represents the predominant isoform expressed in lymphocytes,
whereas PPAR dominates in all cell types of the myeloid lineage.
PPAR expression was down-regulated following T-cell activation while
PPAR expression increased under the same activating conditions.
PPAR expression in T cells may be regulated by microenvironmental
factors, because Peyer's patch T cells expressed far greater levels of
PPAR than T cells isolated from peripheral lymphoid organs. Exposure
to specific ligand determined that PPAR in lymphocytes can
effectively transactivate a peroxisome proliferator response element
reporter construct. PPAR's ability to regulate endogenous genes,
however, required treatment with histone deacetylase inhibitors.
Finally, ligand activation of lymphocyte PPAR antagonized NF-
B.
Our observation that a functional PPAR exists within T cells and B
lymphocytes suggests an expanding role for this nuclear receptor in
cells of the immune system.
*
This work was supported in part by National Institutes of
Health Grants CA25917 and DK55491, by a Browning Foundation grant, and
by Department of Veteran's Affairs Medical Research Funds.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of
Pathology, University of Utah, 30 North 1900 East, Salt Lake City, UT 84132-2501. Tel.: 801-581-3013; Fax: 801-581-8946; E-mail:
daynes.office@path.utah.edu.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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