Abstract
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 language | English |
|---|---|
| Pages (from-to) | 106-113 |
| Number of pages | 8 |
| Journal | Cytokine |
| Volume | 99 |
| DOIs | |
| Publication status | Published - 2017 Nov 1 |
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Keywords
- Autoimmunity
- DC adoptive transfer
- IL-33
- T cell activation
- Th17 cell differentiation
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Biochemistry
- Hematology
- Molecular Biology
Cite this
IL-33-matured dendritic cells promote Th17 cell responses via IL-1β and IL-6. / Park, Su Ho; Kim, Myun Soo; Lim, Hui Xuan; Cho, Dae Ho; Kim, Tae Sung.
In: Cytokine, Vol. 99, 01.11.2017, p. 106-113.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - IL-33-matured dendritic cells promote Th17 cell responses via IL-1β and IL-6
AU - Park, Su Ho
AU - Kim, Myun Soo
AU - Lim, Hui Xuan
AU - Cho, Dae Ho
AU - Kim, Tae Sung
PY - 2017/11/1
Y1 - 2017/11/1
N2 - 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.
AB - 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.
KW - Autoimmunity
KW - DC adoptive transfer
KW - IL-33
KW - T cell activation
KW - Th17 cell differentiation
UR - http://www.scopus.com/inward/record.url?scp=85027871975&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85027871975&partnerID=8YFLogxK
U2 - 10.1016/j.cyto.2017.07.022
DO - 10.1016/j.cyto.2017.07.022
M3 - Article
C2 - 28802996
AN - SCOPUS:85027871975
VL - 99
SP - 106
EP - 113
JO - Cytokine
JF - Cytokine
SN - 1043-4666
ER -