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The Journal of Immunology, 2003, 171: 5743-5750.
Copyright © 2003 by The American Association of Immunologists

Peroxisome Proliferator-Activated Receptor-{gamma}-Deficient Heterozygous Mice Develop an Exacerbated Neural Antigen-Induced Th1 Response and Experimental Allergic Encephalomyelitis 1

John J. Bright2,*, Chandramohan Natarajan*, Gladson Muthian*, Yaavov Barak{dagger} and Ronald M. Evans{dagger}

* Departments of Neurology and Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37212; and {dagger} Gene Expression Laboratory, The Salk Institute, La Jolla, CA 92037

Peroxisome proliferator-activated receptor-{gamma} (PPAR{gamma}) is a nuclear receptor transcription factor that regulates cell growth, differentiation, and homeostasis. PPAR{gamma} agonists are potent therapeutic agents for type 2 diabetes, obesity, and inflammation. Experimental allergic encephalomyelitis (EAE) is a Th1 cell-mediated inflammatory demyelinating autoimmune disease model of multiple sclerosis. We have shown recently that PPAR{gamma} agonists inhibit EAE by blocking IL-12 production, IL-12 signaling, and neural Ag-induced Th1 differentiation. In this study, we show that the PPAR{gamma}-deficient heterozygous mice develop an exacerbated EAE with prolonged clinical symptoms than the wild-type littermates, following immunization with myelin oligodendrocyte glycoprotein (MOG) p35–55 peptide. The exacerbation of EAE in PPAR{gamma}+/- mice associates with an increased expansion of CD4+ and CD8+ T cells and expression of CD40 and MHC class II molecules in response to MOGp35–55 Ag. The PPAR{gamma}+/- mice also showed an increase in T cell proliferation and Th1 response to MOGp35–55 Ag than the wild-type littermates. These findings suggest that PPAR{gamma} be a critical physiological regulator of CNS inflammation and demyelination in EAE and perhaps multiple sclerosis and other Th1 cell-mediated autoimmune diseases.




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