title: Inhibition of autoantigen expression by (-)-epigallocatechin-3-gallate (the major constituent of green tea) in normal human cells.
abstract: Autoimmune disorders, characterized by inflammation and apoptosis of target cells leading to tissue destruction, are mediated in part by autoantibodies against normal cellular components (autoantigens) that may be overexpressed. For example, antibodies against the autoantigens SS-A/Ro and SS-B/La are primary markers for systemic lupus erythematosus and Sjögren's syndrome. Recently, studies in animals demonstrated that green tea consumption may reduce the severity of some autoimmune disorders, but the mechanism is unclear. Herein, we sought to determine whether the most abundant green tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), affects autoantigen expression in human cells. Cultures of pooled normal human primary epidermal keratinocytes and of an immortalized human salivary acinar cell line were incubated with 100 microM EGCG (a physiologically achievable level for topical application or oral administration) for various time periods and then analyzed by cDNA microarray analysis, reverse transcription-polymerase chain reaction, and Western blotting for expression of several major autoantigen candidates. EGCG inhibited the transcription and translation of major autoantigens, including SS-B/La, SS-A/Ro, coilin, DNA topoisomerase I, and alpha-fodrin. These findings, taken together with green tea's anti-inflammatory and antiapoptotic effects, suggest that green tea polyphenols could serve as an important component in novel approaches to combat autoimmune disorders in humans.
authors.affiliation: Department of Oral Biology and Maxillofacial Pathology, School of Dentistry, Medical College of Georgia, Augusta, 30912-1126, USA. shsu@mail.mcg.edu
authors.forename: Stephen
authors.initials: S
authors.lastname: Hsu
authors.forename: Douglas P
authors.initials: DP
authors.lastname: Dickinson
authors.forename: Haiyan
authors.initials: H
authors.lastname: Qin
authors.forename: Carol
authors.initials: C
authors.lastname: Lapp
authors.forename: David
authors.initials: D
authors.lastname: Lapp
authors.forename: James
authors.initials: J
authors.lastname: Borke
authors.forename: Douglas S
authors.initials: DS
authors.lastname: Walsh
authors.forename: Wendy B
authors.initials: WB
authors.lastname: Bollag
authors.forename: Hubert
authors.initials: H
authors.lastname: Stöppler
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Tokio
authors.initials: T
authors.lastname: Osaki
authors.forename: George
authors.initials: G
authors.lastname: Schuster
mesh_terms: D001324:Autoantigens / Q000096:biosynthesis*; D015153:Blotting, Western; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002460:Cell Line; D015536:Down-Regulation / Q000187:drug effects; D006801:Humans; D015603:Keratinocytes / Q000187:drug effects / Q000276:immunology; D020411:Oligonucleotide Array Sequence Analysis; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012469:Salivary Glands / Q000166:cytology / Q000187:drug effects / Q000276:immunology
chemical_list: D001324:Autoantigens; D012313:RNA; D002392:Catechin; C045651:epigallocatechin gallate