Treatment of Psoriasis With Troglitazone Therapy

Pershadsingh, Harrihar A.; Sproul, J.A.; Benjamin, Eugene; Finnegan, J A; Amin, Navin M.

doi:10.1001/archderm.134.10.1304

Cited by 53 publications

(56 citation statements)

References 4 publications

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“…[25][26][27][28][29] Those studies attributed the blockade of macrophage activation and secretion of proinflammatory cytokines as the mechanism of regulation of inflammatory diseases by PPAR␥ agonists. [23][24][25][26][27][28][29][30][31] IL-12 is a macrophage/microglia derived proinflammatory cytokine that plays a crucial role in the pathogenesis of CNS demyelination in EAE/MS. Earlier studies showed that the inhibition of IL-12 production or IL-12 signaling was effective in preventing the clinical and pathological symptoms of EAE.…”

Section: Or Ciglitazone Reduced the Duration And Clinicalmentioning

confidence: 99%

“…Interestingly, recent studies also showed the importance of PPAR␥ in the regulation of immune and inflammatory responses. 23,24 In vivo treatment with PPAR␥ agonists prevent the pathogenesis of rheumatoid arthritis, 25 athero-sclerosis, 26,27 colitis, 28 and psoriasis 29 in animal models, suggesting their potential use for the treatment of human inflammatory diseases. Macrophage has well-established involvement in the inflammatory processes and the natural and synthetic PPAR␥ ligands block macrophage activation and expression of inflammatory cytokines, inducible nitric oxide synthase, gelatinase B and scavenger receptor A gene.…”

Section: Introductionmentioning

confidence: 99%

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Peroxisome proliferator-activated receptor-gamma agonists inhibit experimental allergic encephalomyelitis by blocking IL-12 production, IL-12 signaling and Th1 differentiation

2002

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Peroxisome proliferator-activated receptor-gamma (PPAR␥) is a nuclear receptor transcription factor that regulates or Ciglitazone, decreased the duration and clinical severity of active immunization and adoptive transfer models of EAE. PPAR␥ agonists inhibited EAE in association with a decrease in IL-12 production and differentiation of neural antigen-specific Th1 cells. In vitro treatment of activated T cells with PPAR␥ agonists inhibited IL-12-induced activation of JAK-STAT signaling pathway and Th1 differentiation. These findings highlight the fact that PPAR␥ agonists regulate central nervous system inflammation and demyelination by inhibiting IL-12 production, IL-12 signaling and Th1 differentiation in EAE.

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Section: Or Ciglitazone Reduced the Duration And Clinicalmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Peroxisome proliferator-activated receptor-gamma agonists inhibit experimental allergic encephalomyelitis by blocking IL-12 production, IL-12 signaling and Th1 differentiation

2002

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“…Interestingly, recent studies have also shown that PPAR␥ is an important regulator of immune and inflammatory responses (32,33). In vivo treatment with PPAR␥ agonists inhibits rheumatoid arthritis (34), atherosclerosis (35,36), colitis (37), and psoriasis (38) in animal models, indicating their use for the treatment of human inflammatory diseases (39,40).…”

Section: Ultiple Sclerosis (Ms)mentioning

confidence: 99%

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

Bright

Natarajan

Muthian

et al. 2003

The Journal of Immunology

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Peroxisome proliferator-activated receptor-γ (PPARγ) is a nuclear receptor transcription factor that regulates cell growth, differentiation, and homeostasis. PPARγ 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 PPARγ agonists inhibit EAE by blocking IL-12 production, IL-12 signaling, and neural Ag-induced Th1 differentiation. In this study, we show that the PPARγ-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 PPARγ+/− 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 PPARγ+/− 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 PPARγ 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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“…19 Moreover, PPARg agonists were found to be effective in animals and/or humans in treating the inflammatory diseases colitis, allergic encephalomyelitis, and psoriasis. [79][80][81] PPARb/dÀ/À mice show defects in growth, adipose tissue stores, myelination of the corpus callosum, and wound-healing. 19,82 Any or all of these effects may indicate dysfunction of the inflammatory/immune response.…”

Section: Ppars In Inflammation and Immunitymentioning

confidence: 99%

Peroxisome Proliferator‐Activated Receptors: Potential Therapeutic Targets in Lung Disease?

Denning

Stoll

2005

Pediatric Pulmonology

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The peroxisome proliferator‐activated receptors (PPARs) are a family of nuclear hormone receptors that play central roles in lipid and glucose homeostasis, cellular differentiation, and the immune/inflammatory response. Growing evidence indicates that changes in expression and activation of PPARs likely modulate conditions as diverse as diabetes, atherosclerosis, cancer, asthma, Parkinson's disease, and Alzheimer's disease. Activation of these receptors by natural or pharmacologic ligands leads to both gene‐dependent and gene‐independent effects that alter the expression of a wide array of proteins. In the lung, PPARs are expressed by alveolar macrophages, as well as by epithelial, endothelial, and smooth muscle cells. Studies both in vitro and in vivo suggest that PPAR ligands may have anti‐inflammatory effects in asthma, pulmonary sarcoidosis, and pulmonary alveolar proteinosis, as well as antiproliferative and antiangiogenic effects in epithelial lung cancers. Further studies to understand the contribution of these receptors to health and disease will be important for determining whether they represent a promising target for therapeutic intervention. Pediatr Pulmonol. © 2005 Wiley‐Liss, Inc.

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Treatment of Psoriasis With Troglitazone Therapy

Cited by 53 publications

References 4 publications

Peroxisome proliferator-activated receptor-gamma agonists inhibit experimental allergic encephalomyelitis by blocking IL-12 production, IL-12 signaling and Th1 differentiation

Peroxisome proliferator-activated receptor-gamma agonists inhibit experimental allergic encephalomyelitis by blocking IL-12 production, IL-12 signaling and Th1 differentiation

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

Peroxisome Proliferator‐Activated Receptors: Potential Therapeutic Targets in Lung Disease?

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