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. 2021 May 28;53(5):993–1004. doi: 10.1038/s12276-021-00632-9

Fig. 6. Schematic model of the proposed mechanism.

Fig. 6

TGF-β1 produced by Th17 cells represses the expression of Il12rb2 and Il27ra, leading to reduced surface expression of receptors for IL-12 and IL-27. In the absence of Th17 cell-derived TGF-β1, Th17 cells express increased levels of Il12rb2 and Il27ra, becoming more sensitive to IL-12 and IL-27 signals. Thus, TGF-β1-deficient Th17 cells are more prone to becoming IFN-γ producers, which are more pathogenic in inducing autoimmune inflammation in the CNS and gut. Hence, autocrine TGF-β1 from Th17 cells is critical for maintaining Th17 cell stability and for limiting the pathogenicity of these cells.