Transforming growth factor-beta induces development of the T(H)17 lineage.

By Paul R. Mangan, L. Harrington, Darrell B. O'Quinn, Whitney S. Helms, D. Bullard, C. Elson, R. D. Hatton, S. Wahl, T. Schoeb, C. Weaver. Nature, 2006

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Intestinal bacterial colonization induces mutualistic regulatory T cell responses. (2011, background): “…gut infections drive an inflammatory intestinal CD4+ T cell response with deviation between the different CD4+ T cell subsets (Ivanov et al., 2006; Mangan et al., 2006) and that absent or defective induction of Treg cells in the absence of pathogens can also lead to chronic intestinal Immunity…”
Generation of Pathogenic Th17 Cells in the Absence of TGF-β Signaling (2010, positive): “TGF-β 1 is important for murine Th17 differentiation 7,8 and accordingly, transgenic expression of a mutant TGF-β subunit receptor II (CD4dnTGF β RII) in T cells interferes with the generation of Th17 cells in the setting of EAE 11 .”
The Aryl Hydrocarbon Receptor Regulates Gut Immunity through Modulation of Innate Lymphoid Cells (2011, background): “…abundantly present in the intestinal lamina propria and produce IL-22 and/or IL-17 that are important for mucosal immunity against certain extracel- lular pathogens such as Citrobacter rodentium (Mangan et al., 2006; Ota et al., 2011; Tumanov et al., 2011; Wang et al., 2010; Zheng et al., 2008).”