Document Detail

Novel immunoregulatory properties of EGCG on reducing inflammation in EAE.
MedLine Citation:
PMID:  23276926     Owner:  NLM     Status:  MEDLINE    
EGCG is one of the major catechins in green tea. In this study, we investigated the novel regulatory mechanism of EGCG on amelioration of experimental autoimmune encephalomyelitis (EAE). The data showed that EGCG reduced disease severity in EAE by decreasing brain inflammation and demyelination damage, accompanied by decreased encephalitogenic T cell responses and reduced expression of inflammatory cytokines and chemokines. The effect of EGCG was attributable to its selective inhibition of interferon-gamma and interleukin-17 production in CD4+ T cells, mediated via alteration of the STAT pathway and the transcription factors T-bet and retinoid-related orphan receptor (ROR) gammat/ROR alpha. More important, EGCG has been found novel properties of directly inhibiting Th1 and Th17 cell differentiation in this study. On the other hand, EGCG-treated antigen presenting cells (APC) exhibited reduced co-stimulatory function as a result of altered expression of CD80 and CD86. The results of this study indicate that EGCG is a novel anti-inflammatory agent that could act as a useful drug for the treatment of multiple sclerosis and other neuroinflammatory diseases in the further.
Quanye Sun; Yingxia Zheng; Xia Zhang; Xiaojuan Hu; Yuanxia Wang; Shimin Zhang; Dongqing Zhang; Hong Nie
Related Documents :
23341606 - Jnk inhibition reduces apoptosis and neovascularization in a murine model of age-relate...
23237506 - Regulatory roles of the tumor necrosis factor receptor bcma.
24567866 - β-catenin-mediated inhibition of cross-priming: a new mechanism for tumors to evade im...
24554536 - Matrine-induced apoptosis of human nasopharyngeal carcinoma cells via in vitro vascular...
24819716 - Flll31, a derivative of curcumin, attenuates airway inflammation in a multi-allergen ch...
20843286 - Dehydroepiandrosterone modulates survival and immune functions during sepsis depending ...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2013-01-01
Journal Detail:
Title:  Frontiers in bioscience (Landmark edition)     Volume:  18     ISSN:  1093-4715     ISO Abbreviation:  Front Biosci (Landmark Ed)     Publication Date:  2013  
Date Detail:
Created Date:  2013-01-01     Completed Date:  2013-06-12     Revised Date:  2013-07-29    
Medline Journal Info:
Nlm Unique ID:  101612996     Medline TA:  Front Biosci (Landmark Ed)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  332-42     Citation Subset:  IM    
Shanghai Institute of Immunology, Institutes of Medical Sciences, Shanghai JiaoTong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Antigen-Presenting Cells
CD4-Positive T-Lymphocytes / drug effects,  immunology
Catechin / analogs & derivatives*,  therapeutic use
Cell Differentiation / drug effects
Encephalomyelitis, Autoimmune, Experimental / drug therapy*,  immunology
Mice, Inbred C57BL
Multiple Sclerosis / immunology
STAT Transcription Factors / physiology
Th17 Cells / drug effects
Reg. No./Substance:
0/STAT Transcription Factors; 154-23-4/Catechin; BQM438CTEL/epigallocatechin gallate

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  BlyS: a potential hallmark of multiple myeloma.
Next Document:  Towards elucidating the role of SirT1 in osteoarthritis.