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10.1016/j.jaut.2020.102510

http://scihub22266oqcxt.onion/10.1016/j.jaut.2020.102510
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32622513!7327470!32622513
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suck abstract from ncbi


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pmid32622513      J+Autoimmun 2020 ; 113 (ä): 102510
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  • The roles of PPARgamma and its agonists in autoimmune diseases: A comprehensive review #MMPMID32622513
  • Liu Y; Wang J; Luo S; Zhan Y; Lu Q
  • J Autoimmun 2020[Sep]; 113 (ä): 102510 PMID32622513show ga
  • Autoimmune diseases are common diseases of the immune system that are characterized by the loss of self-tolerance and the production of autoantibodies; the breakdown of immune tolerance and the prolonged inflammatory reaction are undisputedly core steps in the initiation and maintenance of autoimmunity. Peroxisome proliferator-activated receptors (PPARs) are ligand-dependent transcription factors that belong to the nuclear hormone receptor family and act as ligand-activated transcription factors. There are three different isotypes of PPARs: PPARalpha, PPARgamma, and PPARbeta/delta. PPARgamma is an established regulator of glucose homeostasis and lipid metabolism. Recent studies have demonstrated that PPARgamma exhibits anti-inflammatory and anti-fibrotic effects in multiple disease models. PPARgamma can also modulate the activation and polarization of macrophages, regulate the function of dendritic cells and mediate T cell survival, activation, and differentiation. In this review, we summarize the signaling pathways and biological functions of PPARgamma and focus on how PPARgamma and its agonists play protective roles in autoimmune diseases, including autoimmune thyroid diseases, multiple sclerosis, rheumatoid arthritis, systemic sclerosis, systemic lupus erythematosus, primary Sjogren syndrome and primary biliary cirrhosis.
  • |Animals[MESH]
  • |Anti-Inflammatory Agents/*pharmacology/therapeutic use[MESH]
  • |Autoimmune Diseases/drug therapy/*immunology[MESH]
  • |Disease Models, Animal[MESH]
  • |Glucose/metabolism[MESH]
  • |Humans[MESH]
  • |Lipid Metabolism/drug effects/immunology[MESH]
  • |PPAR gamma/agonists/*metabolism[MESH]


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