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. 2019 Sep 13;10:2217. doi: 10.3389/fimmu.2019.02217

Figure 1.

Figure 1

(A) MiR-155 is expressed in plasma (P), monocytes, fibroblast-like synoviocytes (RASF) and synovial fluid monocytes (SFCD14*C) of patients with RA/JIA. It is induced by cytokines and LPS, and overexpression increases chemokine production. SOCS1, IL-13Rα1, and C/EBP-β are key target genes of miR-155. SOCS1 is a negative regulator of STAT1. MiR-155 decreased SOCS1 expression, increasing signaling through STAT1 to promote M1 macrophages and suppress M2 macrophages to promote inflammatory responses. MiR-155 could also directly target C/EBP-β to suppress M2 macrophages. MiR-155 directly targets IL-13Rα1 and decreases the levels of IL-13Ra protein, resulting in decreased activation of the M2-promiting STAT6. MiR-155 is also associated with decreased expression of two predicated miR targets that mediate apoptosis: CASP10 and APAF1. (B) MiR-146a was expressed in PMBCs, monocytes, synovial fibroblasts, and synovial fluid monocytes (SFCD14*C) of patients in RA/JIA. It is induced by cytokines and LPS through the NF-κB pathway. It controls TLR4 signaling through a regulatory loop: the upregulation of miR-146a by caused by activated NF-κB; miR-146a reduces the expression of its targets including TRAF6, IRAK1, IRAK2, and IRF3; which limits activity of both NF-κB and IRF3 pathways.