Received for publication June 3, 2005.
Revised July 20, 2005.
Accepted for publication July 20, 2005.

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 over-expressed. For example, antibodies against the autoantigens SS-A/Ro and SS-B/La are primary markers for systematic lupus erythematosus and Sjoren's syndrome. Recently, studies in animals demonstrated that green tea consumption may reduce the severity of some autoimmune disorders, but the mechanism is unclear. Here, we sought to determine if 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 µM of EGCG (a physiologically achievable level for topical application or oral administration) for various time periods and then analyzed by cDNA microarray analysis, RT-PCR 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 -fodrin. These findings, taken together with green tea's anti-inflammatory and anti-apoptotic effects, suggest that green tea polyphenols could serve as an important component in novel approaches to combat autoimmune disorders in humans.

Key words: Autoantibody, Autoimmune, Lupus, Sjogren's, green tea, polyphenols