Interleukins 1β and 6 but not transforming growth factor-β are essential for the differentiation of interleukin 17–producing human T helper cells
Abstract
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.
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Produced IL-6 further induces Th17 cell differentiation through STAT3 in the presence of TGFβ, IL-1β and IL-23, which are rich in inflammatory lesions and tumor microenvironments.
“The produced IL-6 further induces Th17 cell differentiation through STAT3 in the presence of TGFβ, IL-1β and IL-23, all of which are rich in inflammatory lesions and tumor microenvironments (164, 166, 169–171, 174, 175).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [169]
IL-6, transforming growth factor-b, and IL-1b are required for Th17 differentiation from naïve CD4+ T cells.
“Importantly, IL-6, transforming growth factor-b, and IL-1b are required for Th17 differentiation from naïve CD4þ T cells.56,57”
From Autoimmune diseases and immune-checkpoint inhibitors for cancer therapy: Review of the literature and personalized risk-based prevention strategy (2020) · cites this paper as [56]
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- Authors
- Acosta-Rodriguez, E. V., Napolitani, G., Lanzavecchia, A., & Sallusto, F.
- Affiliations
- Institute for Research in Biomedicine (CH)
- Corresponding author
- Sallusto, Federica
- Venue
- Nature Immunology
- Published
- 2007-08-05
- Volume
- 8
- Issue
- 9
- Pages
- 942-949
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W2012680181
- Cited by
- 1,857
- References
- 43
- Citations by year
- 2026: 43 · 2025: 35 · 2024: 39 · 2023: 47 · 2022: 46 · 2021: 65 · 2020: 63 · 2019: 59 · 2018: 57 · 2017: 93 · 2016: 97 · 2015: 115 · 2014: 119 · 2013: 126 · 2012: 145
- FWCI
- 67.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute for Health and Care Research
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Bundesamt für Gesundheit
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (U19AI057266)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- Th17 cells, IL-17, IL-1β, interleukin-6, TGF-beta, RORγ, CD4+ T cell differentiation, IL-12, antigen-presenting cells, dendritic cells, monocytes, T cell polarization
- MeSH terms
- Antigen-Presenting Cells, Cell Differentiation, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, T-Lymphocytes, Helper-Inducer, Humans, Receptors, Thyroid Hormone, Interleukin-6, T-Lymphocyte Subsets, Cytokines, Transforming Growth Factor beta, Receptors, Retinoic Acid, Interleukin-12, Cell Lineage, Reverse Transcriptase Polymerase Chain Reaction, Interleukin-17, Interleukin-1beta, Nuclear Receptor Subfamily 1, Group F, Member 3
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