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Contrary to popular belief, TGF-β doesn't directly induce Th17 cells. Here, Das et al. show that the cytokine merely paves the way for Th17s by blocking their antagonists.
The consensus among immunologists has been that TGF-β, along with IL-6, is a key ingredient in Th17 cell differentiation. But Das and colleagues find that in the absence of Th1 and Th2 cells, IL-6 alone can do the job. Naive CD4+ T cells from mice lacking the essential Th1 and Th2 transcription factors STAT-6 and T-bet produced copious IL-17 in response to stimulation with IL-6. And adding TFG-β to the mix had no effect.
The double-knockout mice developed severe EAE—an MS-like disease driven by Th17 cells. Their symptoms could be reversed by blocking IL-17 or IL-6, but not by blocking TGF-β. TGF-β inhibited Th1 and Th2 differentiation by downregulating the expression of the essential Th1 and Th2 transcription factors STAT-4 and GATA-3. With the competing subsets shut down, Th17s flourished.