title: Epigallocatechin gallate affects human dendritic cell differentiation and maturation.
abstract: 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.
  
  
  CONCLUSIONS
  Epigallocatechin gallate induces immunosuppressive alterations on human MODCs, both by induction of apoptosis and suppression of cell surface molecules and antigen presentation.
authors.affiliation: Department of Surgical Oncology, Faculty of Medicine, University of Tokyo, Tokyo, Japan. yoneyamas-tky@umin.ac.jp
authors.forename: Satomi
authors.initials: S
authors.lastname: Yoneyama
authors.forename: Kazushige
authors.initials: K
authors.lastname: Kawai
authors.forename: Nelson H
authors.initials: NH
authors.lastname: Tsuno
authors.forename: Yurai
authors.initials: Y
authors.lastname: Okaji
authors.forename: Masahiro
authors.initials: M
authors.lastname: Asakage
authors.forename: Takeshi
authors.initials: T
authors.lastname: Tsuchiya
authors.forename: Jun
authors.initials: J
authors.lastname: Yamada
authors.forename: Eiji
authors.initials: E
authors.lastname: Sunami
authors.forename: Takuya
authors.initials: T
authors.lastname: Osada
authors.forename: Joji
authors.initials: J
authors.lastname: Kitayama
authors.forename: Koki
authors.initials: K
authors.lastname: Takahashi
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Nagawa
mesh_terms: D000938:Antigen-Presenting Cells / Q000187:drug effects*; D017209:Apoptosis / Q000187:drug effects; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects*; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D007165:Immunosuppression Therapy; D016753:Interleukin-10 / Q000378:metabolism; D009000:Monocytes / Q000166:cytology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D016753:Interleukin-10; D002392:Catechin; C045651:epigallocatechin gallate