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Cited by 291

The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.

Peroxisome Proliferator-Activated Receptor-γ Agonist 15-Deoxy-Δ12,1412,14-Prostaglandin J2 Ameliorates Experimental Autoimmune Encephalomyelitis

Diab, Asim, Deng, Caishu, Smith, Jeff D, Hussain, Rehana Z, Phanavanh, Bounleut, Lovett-Racke, Amy E, Drew, Paul D, Racke, Michael K·2002·The Journal of Immunology

Abstract

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-γ expression in the immune system have been limited. Recently, PPAR-γ was identified in monocyte/macrophage cells. In this study we examined the role of PPAR-γ in experimental autoimmune encephalomyelitis (EAE), an animal model for the human disease multiple sclerosis. The hypothesis we are testing is whether PPAR-γ plays an important role in EAE pathogenesis and whether PPAR-γ ligands can inhibit the clinical expression of EAE. Initial studies have shown that the presence of the PPAR-γ ligand 15-deoxy-Δ12,14-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-γ, ΙL-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-γ 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-γ ligands may be a novel therapeutic agent for diseases such as multiple sclerosis.

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Crossref · 10.4049/jimmunol.168.5.2508

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Metadata

Authors
Diab, A., Deng, C., Smith, J. D., Hussain, R. Z., Phanavanh, B., Lovett-Racke, A. E., Drew, P. D., & Racke, M. K.
Venue
The Journal of Immunology
Published
2002-03-01
Volume
168
Issue
5
Pages
2508-2515
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
OpenAlex
W1656162023
Cited by
291
References
39
FWCI
14.50
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Peroxisome Proliferator-Activated Receptor-γ Agonist 15-Deoxy-Δ12,1412,14-Prostaglandin J2 Ameliorates Experimental Autoimmune Encephalomyelitis. https://app.cochat.ai/papers/10.4049/jimmunol.168.5.2508
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Diab, A., Deng, C., Smith, J. D., Hussain, R. Z., Phanavanh, B., Lovett-Racke, A. E., Drew, P. D., & Racke, M. K. (2002). Peroxisome Proliferator-Activated Receptor-γ Agonist 15-Deoxy-Δ12,1412,14-Prostaglandin J2 Ameliorates Experimental Autoimmune Encephalomyelitis. The Journal of Immunology. https://doi.org/10.4049/jimmunol.168.5.2508

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