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Agonist 15-Deoxy-
12,1412,14-Prostaglandin J2 Ameliorates Experimental Autoimmune Encephalomyelitis1
*
Department of Neurology and
Center for Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390; and
Department of Anatomy and Neurobiology, University of Arkansas for Medical Sciences, Little Rock, AR 72205
Peroxisome proliferator-activated receptors (PPAR) are members of a
nuclear hormone receptor superfamily that includes receptors for
steroids, retinoids, and thyroid hormone, all of which are known to
affect the immune response. Previous studies dealing with PPAR-
expression in the immune system have been limited. Recently, PPAR-
was identified in monocyte/macrophage cells. In this study we examined
the role of PPAR- in experimental autoimmune encephalomyelitis
(EAE), an animal model for the human disease multiple sclerosis. The
hypothesis we are testing is whether PPAR- plays an important role
in EAE pathogenesis and whether PPAR- ligands can inhibit the
clinical expression of EAE. Initial studies have shown that the
presence of the PPAR- ligand
15-deoxy-
12,14-PGJ2 (15d-PGJ2) inhibits the
proliferation of Ag-specific T cells from the spleen of myelin basic
protein Ac1–11 TCR-transgenic mice. 15d-PGJ2 suppressed
IFN-, IL-10, and IL-4 production by both Con A- and myelin basic
protein Ac1–11 peptide-stimulated lymphocytes as
determined by ELISA and ELISPOT assay. Culture of encephalitogenic T
cells with 15d-PGJ2 in the presence of Ag reduced the ability of these
cells to adoptively transfer EAE. Examination of the target organ, the
CNS, during the course of EAE revealed expression of PPAR- in the
spinal cord inflammatory infiltrate. Administration of 15d-PGJ2 before
and at the onset of clinical signs of EAE significantly reduced the
severity of disease. These results suggest that PPAR- ligands may be
a novel therapeutic agent for diseases such as multiple
sclerosis.
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