PMID- 17935769
OWN - NLM
STAT- MEDLINE
DCOM- 20080225
LR  - 20211203
IS  - 1097-6825 (Electronic)
IS  - 0091-6749 (Linking)
VI  - 121
IP  - 1
DP  - 2008 Jan
TI  - Epigallocatechin gallate affects human dendritic cell differentiation and 
      maturation.
PG  - 209-14
AB  - 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.
FAU - Yoneyama, Satomi
AU  - Yoneyama S
AD  - Department of Surgical Oncology, Faculty of Medicine, University of Tokyo, Tokyo, 
      Japan. yoneyamas-tky@umin.ac.jp
FAU - Kawai, Kazushige
AU  - Kawai K
FAU - Tsuno, Nelson H
AU  - Tsuno NH
FAU - Okaji, Yurai
AU  - Okaji Y
FAU - Asakage, Masahiro
AU  - Asakage M
FAU - Tsuchiya, Takeshi
AU  - Tsuchiya T
FAU - Yamada, Jun
AU  - Yamada J
FAU - Sunami, Eiji
AU  - Sunami E
FAU - Osada, Takuya
AU  - Osada T
FAU - Kitayama, Joji
AU  - Kitayama J
FAU - Takahashi, Koki
AU  - Takahashi K
FAU - Nagawa, Hirokazu
AU  - Nagawa H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20071101
PL  - United States
TA  - J Allergy Clin Immunol
JT  - The Journal of allergy and clinical immunology
JID - 1275002
RN  - 130068-27-8 (Interleukin-10)
RN  - 8R1V1STN48 (Catechin)
RN  - BQM438CTEL (epigallocatechin gallate)
SB  - IM
MH  - Antigen-Presenting Cells/*drug effects
MH  - Apoptosis/drug effects
MH  - Catechin/*analogs & derivatives/pharmacology
MH  - Cell Differentiation/*drug effects
MH  - Cells, Cultured
MH  - Dendritic Cells/cytology/*drug effects/physiology
MH  - Humans
MH  - *Immunosuppression Therapy
MH  - Interleukin-10/metabolism
MH  - Monocytes/cytology
MH  - T-Lymphocytes/immunology
EDAT- 2007/10/16 09:00
MHDA- 2008/02/26 09:00
CRDT- 2007/10/16 09:00
PHST- 2007/02/09 00:00 [received]
PHST- 2007/08/06 00:00 [revised]
PHST- 2007/08/08 00:00 [accepted]
PHST- 2007/10/16 09:00 [pubmed]
PHST- 2008/02/26 09:00 [medline]
PHST- 2007/10/16 09:00 [entrez]
AID - S0091-6749(07)01592-8 [pii]
AID - 10.1016/j.jaci.2007.08.026 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol. 2008 Jan;121(1):209-14. doi: 10.1016/j.jaci.2007.08.026. 
      Epub 2007 Nov 1.