Interleukins 1beta and 6 but not transforming growth factor-beta are critical cytokines for induction of human Th17 cells

ACOSTA RODRIGUEZ EV; NAPOLITANI G; LANZAVECCHIA A; SALLUSTO F

NATURE IMMUNOLOGY (PRINT)

Año: 2007 p. 942 - 949

1529-2908

Interleukin 17 (IL-17)?producing CD4+ helper T cells (TH-17 cells) have been linked to host defense and autoimmune diseases. In mice, the differentiation of TH-17 cells requires transforming growth factor-b and IL-6 and the transcription factor RORct. We report here that for human naive CD4+ T cells, RORct expression and TH-17 polarization were induced by IL-1b and enhanced by IL-6 but were suppressed by transforming growth factor-b and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced TH-17 priming, and this function correlated with antigen-presenting cell production of IL-1b and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.+ helper T cells (TH-17 cells) have been linked to host defense and autoimmune diseases. In mice, the differentiation of TH-17 cells requires transforming growth factor-b and IL-6 and the transcription factor RORct. We report here that for human naive CD4+ T cells, RORct expression and TH-17 polarization were induced by IL-1b and enhanced by IL-6 but were suppressed by transforming growth factor-b and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced TH-17 priming, and this function correlated with antigen-presenting cell production of IL-1b and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.H-17 cells requires transforming growth factor-b and IL-6 and the transcription factor RORct. We report here that for human naive CD4+ T cells, RORct expression and TH-17 polarization were induced by IL-1b and enhanced by IL-6 but were suppressed by transforming growth factor-b and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced TH-17 priming, and this function correlated with antigen-presenting cell production of IL-1b and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.+ T cells, RORct expression and TH-17 polarization were induced by IL-1b and enhanced by IL-6 but were suppressed by transforming growth factor-b and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced TH-17 priming, and this function correlated with antigen-presenting cell production of IL-1b and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.b and IL-12. Monocytes and conventional dendritic cells, but not monocyte-derived dendritic cells activated by microbial stimuli, efficiently induced TH-17 priming, and this function correlated with antigen-presenting cell production of IL-1b and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.H-17 priming, and this function correlated with antigen-presenting cell production of IL-1b and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.b and IL-6 but not IL-12. Our results identify cytokines, antigen-presenting cells and microbial products that promote the polarization of human TH-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.H-17 cells and emphasize an important difference in the requirements for the differentiation of TH-17 cells in humans and mice.H-17 cells in humans and mice.