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      TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells.

      Immunity

      physiology, Transforming Growth Factor beta1, immunology, metabolism, Cell Differentiation, Cells, Cultured, Cytokines, Dendritic Cells, cytology, Interleukin-17, biosynthesis, Lymphocyte Subsets, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Receptors, Interleukin-1, Smad7 Protein, T-Lymphocytes, T-Lymphocytes, Regulatory, Th1 Cells, Th2 Cells, Transforming Growth Factor beta, Animals, CD4-Positive T-Lymphocytes

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          Abstract

          We describe de novo generation of IL-17-producing T cells from naive CD4 T cells, induced in cocultures of naive CD4 T cells and naturally occurring CD4+ CD25+ T cells (Treg) in the presence of TLR3, TLR4, or TLR9 stimuli. Treg can be substituted by TGFbeta1, which, together with the proinflammatory cytokine IL-6, supports the differentiation of IL-17-producing T cells, a process that is amplified by IL-1beta and TNFalpha. We could not detect a role for IL-23 in the differentiation of IL-17-producing T cells but confirmed its importance for their survival and expansion. Transcription factors GATA-3 and T-bet, as well as its target Hlx, are absent in IL-17-producing T cells, and they do not express the negative regulator for TGFbeta signaling, Smad7. Our data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation of IL-17-producing T cells.

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          Journal
          10.1016/j.immuni.2006.01.001
          16473830

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