Details

Autor(en) / Beteiligte

• Yoneyama, Satomi, MD
• Kawai, Kazushige, MD
• Tsuno, Nelson H., MD
• Okaji, Yurai, MD
• Asakage, Masahiro, MD
• Tsuchiya, Takeshi, MD
• Yamada, Jun, MD
• Sunami, Eiji, MD
• Osada, Takuya, MD
• Kitayama, Joji, MD
• Takahashi, Koki, MD
• Nagawa, Hirokazu, MD

Titel

Epigallocatechin gallate affects human dendritic cell differentiation and maturation

Ist Teil von

• Journal of allergy and clinical immunology, 2008, Vol.121 (1), p.209-214

Ort / Verlag

New York, NY: Mosby, Inc

Erscheinungsjahr

2008

Quelle

MEDLINE

Beschreibungen/Notizen

• Background Epigallocatechin gallate (EGCG), a component of green tea catechin with the strongest biological activity, has been focused in recent years because of its anti-inflammatory and immunomodulatory activities. Dendritic cells (DCs) are professional antigen-presenting cells, capable of priming naive T cells, and play the key roles in the activation of T-cell–mediated immune responses. Objective We aimed to investigate the effect of EGCG on human monocyte-derived DCs (MODCs) and, consequently, on the T-cell–mediated immune response. Methods The induction of apoptosis, and the detailed phenotypic and functional changes of MODCs, generated by culture of peripheral blood monocytes in the presence of GM-CSF and IL-4, induced by EGCG was investigated and compared with the effects of dexamethasone. Results Epigallocatechin gallate induced apoptosis and affected the phenotype of the developing DCs. The expressions of CD83, CD80, CD11c, and MHC class II, which are molecules essential for antigen presentation by DCs, were downregulated by EGCG. EGCG also suppressed the endocytotic ability of immature DCs, whereas dexamethasone-treated DCs had higher endocytotic ability than control DCs. Most importantly, mature DCs treated with EGCG inhibited stimulatory activity toward allogeneic T cells while secreting high amounts of IL-10. Conclusion Epigallocatechin gallate induces immunosuppressive alterations on human MODCs, both by induction of apoptosis and suppression of cell surface molecules and antigen presentation.