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

Original publication

DOI

10.1038/ni1496

Type

Journal article

Journal

Nat Immunol

Publication Date

09/2007

Volume

8

Pages

942 - 949

Keywords

Antigen-Presenting Cells, Cell Differentiation, Cell Lineage, Cells, Cultured, Cytokines, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Humans, Interleukin-12, Interleukin-17, Interleukin-1beta, Interleukin-6, Nuclear Receptor Subfamily 1, Group F, Member 3, Receptors, Retinoic Acid, Receptors, Thyroid Hormone, Reverse Transcriptase Polymerase Chain Reaction, T-Lymphocyte Subsets, T-Lymphocytes, Helper-Inducer, Transforming Growth Factor beta