Fig. 2: TGFβ1 signaling maintains Ahr expression in TH17 cells, while it opposes IL-23-driven conversion into pathogenic TH17 cells. | Cell Death & Disease

Fig. 2: TGFβ1 signaling maintains Ahr expression in TH17 cells, while it opposes IL-23-driven conversion into pathogenic TH17 cells.

From: TGFβ1 signaling sustains aryl hydrocarbon receptor (AHR) expression and restrains the pathogenic potential of TH17 cells by an AHR-independent mechanism

Fig. 2

a Naive CD4+ T cells were cultured 3 days under nonpathogenic TH17-polarizing conditions (TGFβ1+IL-6) in the absence or presence of FICZ and then stained intracellularly for IL-17A and IL-22 (first culture). A fraction of recovered cells cultured without FICZ was re-stimulated for additional 3 days with TGFβ1, IL-6 plus IL-23, or only IL-23, with or without FICZ stimulation (second culture). b Frequencies of IL-17A+ and IL-22+ cells after the second culture shown in a. c qPCR analysis of Ahr, Cyp1a1, Ahrr, Il17a, and Tbx21 of naive CD4+ T cells cultured under nonpathogenic TH17-polarizing conditions (TGFβ1+IL-6) for 3 days (first culture, white bars) and re-stimulated with TGFβ1, IL-6, and IL-23 combinations for 24 h (second culture). NS not significant; *P < 0.05, **P < 0.01, and ***P < 0.001 (two-way ANOVA)

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