HMOC, a chrysin derivative, induces tolerogenic properties in lipopolysaccharide-stimulated dendritic cells
- Authors
- Song, Ha-Yeon; Kim, Woo Sik; Han, Jeong Moo; Park, Woo Yong; Lim, Seung-Taik; Byun, Eui-Baek
- Issue Date
- 6월-2021
- Publisher
- ELSEVIER
- Keywords
- 3-Dioxygenase; Chrysin derivative; Indoleamine 2; Regulatory T cells; Tolerogenic dendritic cells
- Citation
- INTERNATIONAL IMMUNOPHARMACOLOGY, v.95
- Indexed
- SCIE
SCOPUS
- Journal Title
- INTERNATIONAL IMMUNOPHARMACOLOGY
- Volume
- 95
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/137319
- DOI
- 10.1016/j.intimp.2021.107523
- ISSN
- 1567-5769
- Abstract
- Although we previously identified a new hydroxymethoxyl chrysin derivative (HMOC) using ionizing radiation, the anti-inflammatory mechanism of HMOC in dendritic cells remains unclear. In this study, we investigate the effects of HMOC on phenotypic and functional changes in activated bone marrow-derived dendritic cells (BMDCs). In lipopolysaccharide (LPS)-stimulated BMDCs, HMOC treatment inhibited pro-inflammatory cytokines (TNF-alpha, IL-12p70, and IL-1 beta), surface molecules (CD80, CD86, MHC-I, and MHC-II), and antigenpresentation to MHC-I and II without a decrease in IL-10. Furthermore, HMOC increased indoleamine 2,3-dioxygenase-1 (IDO1) activity via activation of JNK and p38 signaling in the presence of LPS. Interestingly, LPSstimulated DCs treated with HMOC inhibited the proliferation and activation of CD4+ and CD8+ T cells, as well as differentiation of CD4+ T cells into Th1-, Th2- and Th17 cells. In addition, LPS-stimulated DCs treated with HMOC induced an increase in CD4+CD25+Foxp3+ regulatory T cells (Tregs). Collectively, our results suggest that HMOC confers tolerogenic properties in BMDCs, which are responsible for inducing Th cell differentiation to Tregs. Our findings provide a better understanding of the anti-inflammatory mechanism of HMOC in DCs and may contribute to development of a valuable therapeutic candidate for atopic dermatitis.
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Collections - Graduate School > Department of Biotechnology > 1. Journal Articles
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