IL-33-matured dendritic cells promote Th17 cell responses via IL-1β and IL-6

[Display omitted] •IL33 enhances Th17 cell differentiation through DC maturation.•IL33 does not directly induce differentiation of naïve CD4+ T cells to Th17 cells.•IL33-matDCs increase surface molecule-expressions driving T cell activation.•IL33-matDCs promote Th17 cell responses via DC-derived IL-...

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Veröffentlicht in:Cytokine (Philadelphia, Pa.) Pa.), 2017-11, Vol.99, p.106-113
Hauptverfasser: Park, Su-Ho, Kim, Myun Soo, Lim, Hui Xuan, Cho, Daeho, Kim, Tae Sung
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Sprache:eng
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Zusammenfassung:[Display omitted] •IL33 enhances Th17 cell differentiation through DC maturation.•IL33 does not directly induce differentiation of naïve CD4+ T cells to Th17 cells.•IL33-matDCs increase surface molecule-expressions driving T cell activation.•IL33-matDCs promote Th17 cell responses via DC-derived IL-1β and IL-6. IL-33 is associated with a variety of autoimmune diseases, such as sclerosis, inflammatory bowel disease, and rheumatoid arthritis. Although IL-33 is mainly involved in the induction of Th2 cells, however, the relationship between IL-33 and Th17 cells is still largely unknown. In this study, we investigated the effects of IL-33 on DC-mediated CD4+ T cell activation and Th17 cell differentiation because DCs are essential cells for presenting self-antigens to CD4+ T cells in autoimmune disease conditions. OT-II mice were injected with IL-33-treated DCs or untreated DCs that were primed by OVA323-339 peptide, and their Th17 cell responses were compared. Th17 cell population and IL-17 expression levels were significantly increased in draining lymph nodes of mice injected with IL-33-treated DCs, compared with those in mice injected with untreated DCs. IL-33 treatment maturated DCs to present self-antigens and to increase production of proinflammatory cytokines such as IL-1β and IL-6, which have a crucial role in Th17 cell differentiation. We found that the IL-33-matured DCs enhanced the expression of an early T cell activation marker (CD69) and the Th17 master transcription factor (RORγt), but IL-33 did not directly affect CD4+ T cell differentiation or increase Th17 polarization. Notably, neutralizing IL-1β and/or IL-6 significantly decreased IL-17 expression levels and Th17 cell population which were increased by the coculture of CD4+ T cells with IL-33-matured DCs, indicating that IL-33 may induce Th17 cell responses via IL-1β and IL-6 derived from IL-33-matured DCs.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2017.07.022