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. 2020 Jun 22;10(6):937. doi: 10.3390/biom10060937

Figure 2.

Figure 2

MiR-145 is decreased in SLE patients. MiR-145 has a role in the inhibition of STAT1, which is involved in the differentiation of Treg cells via its inhibition of Foxp3. Moreover, STAT1 induces T-bet, which participates in the differentiation of Th1 cells [36]. MiR-410 is downregulated in SLE patients and is a suppressor of STAT3. STAT3 is an inducer of IL-10. The levels of this cytokine are increased in SLE patients, leading to the enhanced survival and differentiation of B cells and the increased production of antibodies [37]. MiR-224 is increased in SLE patients and has been shown to inhibit API5. API5 decreases the expression of APAF1 and precludes the activation of caspases, thereby hampering apoptosome formation. Thus, the over-expression of miR-224 leads to increased T cell activation-induced cell death [36]. MiR-29a is upregulated in SLE patients and suppresses Sp1, which is an inducer of ANMT1. The over-expression of miR-29a leads to hypomethylation of CD11a and CD70, which are involved in the production of autoreactive T cells [38] Abbreviations: Treg cell: Regulatory T cell, DNMT1: DNA (cytosine-5)-methyltransferase 1, SP1: specificity protein 1.