Abstract
The effects of epigallocatechin-3-gallate (EGCG) on dendritic cells (DC) maturation were investigated. EGCG, in a dose-dependent manner, profoundly inhibited CD80, CD86, and MHC class I and II expression on bone marrow-derived murine myeloid DC. EGCG restored the decreased dextran-FITC uptake and inhibited enhanced IL-12 production by LPS-treated DC. EGCG-treated DC were poor stimulators of naïve allogeneic T-cell proliferation and reduced levels of IL-2 production in responding T cells. EGCG-pretreated DC inhibited LPS-induced MAPKs, such as ERK1/2, p38, JNK, and NF-κB p65 translocation. Therefore, the molecular mechanisms by which EGCG antagonized LPS-induced DC maturation appeared to involve the inhibition of MAPK and NF-κB activation. These novel findings provide new insight into the immunopharmacological role of EGCG and suggest a novel approach to the manipulation of DC for therapeutic application of autoimmune and allergic diseases.
| Original language | English |
|---|---|
| Pages (from-to) | 148-155 |
| Number of pages | 8 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 313 |
| Issue number | 1 |
| DOIs | |
| State | Published - 2004.01.2 |
Keywords
- Dendritic cell
- Epigallocatechin-3-gallate
- Mitogen-activated protein kinases
- NF-κB
Quacquarelli Symonds(QS) Subject Topics
- Biological Sciences
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