Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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




Journal article


Nat Immunol

Publication Date





942 - 949


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