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. Author manuscript; available in PMC: 2009 Jun 15.
Published in final edited form as: Semin Immunol. 2007 Nov 28;19(6):409–417. doi: 10.1016/j.smim.2007.10.011

Figure 2. Cytokine pathways and transcription factors in murine Th17 and Treg cell differentiation.

Figure 2

RORγt and Foxp3 are central factors in Th17 and Treg cell differentiation, respectively. Th17 inducing cytokines (in green) induce RORγt through STAT3 (IL-6, IL-21, and IL-23) and IRF4 (induced by TCR activation). However, none of the RORγt-inducing cytokines can induce Th17 differentiation in the absence of TGF-β signaling. Th17 suppressing cytokines (in red) act in several ways. IL-2 acts through STAT5, and IL-27 possibly through SOCS3 and STAT3, inhibiting RORγt-upregulation. Retinoic acid (RA), which promotes Treg development, and TGF-β by itself, which induces Foxp3 expression, decrease Th17 differentiation. In addition, Th1 and Th2 inducing cytokines, such as IL-4, IFNγ, and IL-25 also inhibit Th17 differentiation by unknown mechanisms. TGF-β thus plays a dual role by being absolutely required for Th17 cell differentiation and by also promoting Treg cell development.