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. 2020 Dec 2;11:608900. doi: 10.3389/fimmu.2020.608900

Figure 1.

Figure 1

The interplay between Th17 and Tr1 cells in inflammation. Ahr, c-Maf, and Blimp-1 promote the differentiation of Tr1 cells in response to IL-10, IL-21, and IL-27 via STAT3 activation. IL-27 was found to be sufficient to induce Blimp-1 in Tr1 cells and sustain high IL-10 production. IL-23 supresses Tr1 cells. Early Th17 cell development is initiated by TGF-B and IL-6, inducing IL-23R expression and IL-17 production. IL-23 signaling regulates Th17 cells and their pathogenicity. STAT-3 mediated IL-23-dependent Blimp-1 enhances Th17 pathogenic factors by increasing IL-23R expression, GM-CSF, IFN-y and repressing IL-2. RORγt expression is stabilized by IL-23R expression. IL-27 supresses Th17 cells. Memory T cells in response to TLR signaling produce IL-23. Memory T cells with Th17 pro-inflammatory phenotype secrete large amounts of 17A, IL-17F and IL-22.