Prevention of autoimmune diabetes in NOD mice by troglitazone is associated with modulation of ICAM-1 expression on pancreatic islet cells and IFN-γ expression in splenic T cells

Augstein, Petra; Dunger, A; Heinke, P.; Wachlin, Gerhild; Berg, Sabine; Hehmke, B; Salzsieder, Eckhard

doi:10.1016/s0006-291x(03)00590-4

Cited by 39 publications

(29 citation statements)

References 63 publications

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“…These findings were further confirmed by other groups (9,10) and another thiazolidinedione was also reported to prevent the type 1 diabetes (11,12). It was proposed that thiazolidinediones might be considered for β cell protection in LADA patients (12).…”

Section: Recently Maruyama Et Al Showed That a Low Dose Of Insulin Asupporting

confidence: 70%

Pioglitazone Might Prevent the Progression of Slowly Progressive Type 1 Diabetes

et al. 2009

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Section: Recently Maruyama Et Al Showed That a Low Dose Of Insulin Asupporting

confidence: 70%

Pioglitazone Might Prevent the Progression of Slowly Progressive Type 1 Diabetes

et al. 2009

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“…Other studies have reported that thiazolidinediones possess anti-inflammatory properties and decrease diabetes incidence in nonobese diabetic (NOD) mice (22,23). Prevention of autoimmune diabetes in NOD mice by thiazolidinediones has been associated with suppression of intercellular adhesion molecule 1 (ICAM1) expression and alteration of Th1/Th2 cytokine balance (24). Interestingly, we have recently reported (25) an association of the Gly241Arg polymorphism of ICAM1 with type 1 diabetes.…”

mentioning

confidence: 90%

Analysis of the Type 2 Diabetes-Associated Single Nucleotide Polymorphisms in the Genes IRS1, KCNJ11, and PPARG2 in Type 1 Diabetes

et al. 2004

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It has been proposed that type 1 and 2 diabetes might share common pathophysiological pathways and, to some extent, genetic background. However, to date there has been no convincing data to establish a molecular genetic link between them. We have genotyped three single nucleotide polymorphisms associated with type 2 diabetes in a large type 1 diabetic family collection of European descent: Gly972Arg in the insulin receptor substrate 1 (IRS1) gene, Glu23Lys in the potassium inwardly-rectifying channel gene (KCNJ11), and Pro12Ala in the peroxisome proliferative-activated receptor ␥2 gene (PPARG2). We were unable to confirm a recently published association of the IRS1 Gly972Arg variant with type 1 diabetes. Moreover, KCNJ11 Glu23Lys showed no association with type 1 diabetes (P > 0.05). However, the PPARG2 Pro12Ala variant showed evidence of association (RR 1.15, 95% CI 1.04 -1.28, P ‫؍‬ 0.008). Additional studies need to be conducted to confirm this result. Diabetes 53: 870 -873, 2004

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“…IFN-␥ is also a major effector cytokine, responsible for driving cell-mediated immunity and mediating organ-specific autoimmunity (32). Recent studies have shown that PPAR␥ ligands inhibit IFN-␥ production by T lymphocytes; however, the mechanism underlying this observation has not been clarified (4,6,16,21,(33)(34)(35)(36). Based on previous studies, PPAR␥ ligands could indirectly decrease IFN-␥ by inhibiting activation of T cells, production of IL-2, or induction of apoptosis (3,5,8), or inhibiting IL-12 production by APCs (37)(38)(39)(40).…”

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confidence: 99%

Repression of IFN-γ Expression by Peroxisome Proliferator-Activated Receptor γ

Cunard

Eto

Muljadi

et al. 2004

The Journal of Immunology

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Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors expressed in a wide variety of cells. Our studies and others have demonstrated that both human and murine T cells express PPARγ and that expression can be augmented over time in mitogen-activated splenocytes. PPARγ ligands decrease proliferation and IL-2 production, and induce apoptosis in both B and T cells. PPARγ ligands have also been shown to be anti-inflammatory in multiple models of inflammatory disease. In the following study, we demonstrate for the first time that PPARγ is expressed in both murine CD4 and CD8 cells and that PPARγ ligands directly decrease IFN-γ expression by murine and transformed T cell lines. Unexpectedly, GW9662, a PPARγ antagonist, increases lymphocyte IFN-γ expression. Transient transfection studies reveal that PPARγ ligands, in a PPARγ-dependent manner, potently repress an IFN-γ promoter construct. Repression localizes to the distal conserved sequence of the IFN-γ promoter. Our studies also demonstrate that PPARγ acts on the IFN-γ promoter by interfering with c-Jun activation. These studies suggest that many of the observed anti-inflammatory effects of PPARγ ligands may be related to direct inhibition of IFN-γ by PPARγ.

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Prevention of autoimmune diabetes in NOD mice by troglitazone is associated with modulation of ICAM-1 expression on pancreatic islet cells and IFN-γ expression in splenic T cells

Cited by 39 publications

References 63 publications

Pioglitazone Might Prevent the Progression of Slowly Progressive Type 1 Diabetes

Pioglitazone Might Prevent the Progression of Slowly Progressive Type 1 Diabetes

Analysis of the Type 2 Diabetes-Associated Single Nucleotide Polymorphisms in the Genes IRS1, KCNJ11, and PPARG2 in Type 1 Diabetes

Repression of IFN-γ Expression by Peroxisome Proliferator-Activated Receptor γ

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