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- W4313387776 abstract "Abstract Ligands for the nuclear hormone receptor PPARγ, which are used to treat human type 2 diabetes, also down-regulate APCs and pathogenic T cells. While these effects may underlie the recent demonstration of the efficacy of PPARγ ligands in treating autoimmunity, a role for PPARγ in CD4+CD25+ natural regulatory T cells (TR) has not yet been examined. Strikingly, we found that murine ex-vivo TR express 10-fold higher levels of PPARγ than naive CD4+CD25− T cells (Teff). To examine whether the immunotherapeutic effects of the synthetic PPARγ ligand Ciglitazone (Cgl) involve TR we used the C57BL/6 (WT) Teff → bm12 model of GVHD. Neither ex-vivo TR alone nor Cgl alone was capable of preventing disease. However, Cgl administered with TR significantly ameliorated GVHD. We generated mice with PPARγ-null T cells (T-PPAR) and found that T-PPAR TR were unable to mediate Cgl’s effect. Thus, PPARγ-expressing TR are required for Cgl’s immunotherapeutic effect. We next asked if PPARγ signaling via endogenous ligands, in the absence of synthetic ligands, might also play an important role in TR function. Transfer of in-vitro activated WT TR significantly ameliorated GVHD, with 90% of bm12 mice surviving the disease. In contrast, activated T-PPAR TR were significantly less effective in suppressing disease, with only 40% of bm12 mice surviving. Overall, our results demonstrate for the first time an integral role for PPARγ in TR function." @default.
- W4313387776 created "2023-01-06" @default.
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- W4313387776 date "2007-04-01" @default.
- W4313387776 modified "2023-09-27" @default.
- W4313387776 title "How PPARγ Mediates Immunoregulation: An Integral Role for PPARγ in Regulatory T cells (131.6)" @default.
- W4313387776 doi "https://doi.org/10.4049/jimmunol.178.supp.131.6" @default.
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