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. 2020 Jul 1;113:102510. doi: 10.1016/j.jaut.2020.102510

Fig. 3.

Fig. 3

Protective roles of PPARγ involved in autoimmune diseases. Activation of PPARγcan downregulate the expression of CXCL10 and CXCL11 in thyrocytes; decrease the expression of CXCR3 and CXCL9 in endothelial cells and inhibit the angiogenesis process; inhibit TGF-β, HA and HAS3 in myoblasts; promote the proliferation and fucntion of Tregs and suppress the differentiation and function of Th17 cells, induce apoptosis of Th cells via inhibit the expression of Bcl-2; decrease the production of autoantibodies; promote the differentiation of M2 phenotype of macrophages and the tolergenic DCs; induce the apoptosis of synovial cells; repress the NF-κB signaling pathway in FLSs and inhibit the migration and proliferation of FLSs; suppress the TGF-β induced collagen genes expression, the differentiation of myofibroblasts, the Smad-dependent promoter activity in fibroblasts, and inhibit the proliferation and viability of fibroblasts while induce the apoptosis of fibroblasts; suppress the IL-1β and NF-κB signaling pathways in SGECs and inhibit the apoptosis of SGECs; inhibit the IL-1β pathway in lacrimal gland acinar cells; decrease the levels of IL-6, TNF-α and IL-1βwhile increase the level of IL-4 in the serum. Thus, activation of PPARγcan inhibit the inflammatory reactions, modulate the balance between immune cells and protect the target organs in autoimmune diseases. Symbols: + enhance,- suppress. Abbreviations: PPARγ, Peroxisome proliferator-activated receptor γ; HA, hyaluronan; TGF-β, transforming growth factor β; IL, interleukin; TNF-α, tumor necrosis factor α; IFN-γ, interferon γ; CXCR, chemokine receptor; CXCL, chemokine (C-X-C motif) ligand; Th, T helper cells; Treg, regulatory T cells; miR, microRNA; NF-κB: nuclear transcription factor-κB; FLSs, fibroblast-like synoviocytes; SGECs, salivary gland epithelial cells; DCs, dendritic cells.