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

Su Ho Park, Myun Soo Kim, Hui Xuan Lim, Daeho Cho, Tae Sung Kim

Research output: Contribution to journalArticlepeer-review

39 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)106-113
Number of pages8
Publication statusPublished - 2017 Nov

Bibliographical note

Funding Information:
This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (Minister of Science, ICT and Future Planning) (Creative Materials Discovery Program 2016M3D1A1021387 ) ( NRF-2017R1A2B2009442 ), and also by a Korea University grant (to T.S. Kim). S.-H. Park was supported by Global PhD Fellowship Program through the National Research Foundation of Korea funded by the Ministry of Education ( 2015H1A2A1031021 ).

Publisher Copyright:
© 2017 Elsevier Ltd


  • Autoimmunity
  • DC adoptive transfer
  • IL-33
  • T cell activation
  • Th17 cell differentiation

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Biochemistry
  • Hematology
  • Molecular Biology


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