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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #208783
Title: Green tea catechin EGCG suppresses T cell-mediated function through inhibiting cell division and reducing cell survival

Author
item WU, DAYONG - TUFTS/HNRCA
item GUO, ZHUYAN - TUFTS/HNRCA
item REN, ZHIHONG - TUFTS/HNRCA
item Meydani, Simin

Submitted to: Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 2/6/2007
Publication Date: 4/3/2007
Citation: Wu, D., Guo, Z., Ren, Z., Meydani, S. 2007. Green tea catechin EGCG suppresses T cell-mediated function through inhibiting cell division and reducing cell survival. Experimental Biology/The FASEB Journal. 21(6):p. A738.

Interpretive Summary:

Technical Abstract: Green tea and its active ingredient, epigallocatechin-3-gallate (EGCG), have been indicated to have varied health benefits. Given the rapid increase in consumption of green tea, particularly the high intakes from supplements, its potential risks need to be evaluated. To date, little is known about the effect of green tea on immune response. However, the limited information available suggests an immuno-suppressive and anti-inflammatory property of green tea EGCG. We previously showed that in vitro supplementation with EGCG at physiologically relevant levels (2.5 to 10 microM) inhibited T cell proliferation. Thus, we conducted a study to determine the underlying mechanisms using in vitro supplementation of spleen cells from C57BL mice. Our results showed that EGCG dose-dependently (2.5 to 20 microM) inhibited cell division of stimulated T cells, as monitored by FACS analysis using tracking dye CFSE, and increased late but not early apoptosis of T cells as indicated by the characteristics of Annexin V and 7-AAD staining. Furthermore, EGCG dose-dependently reduced intracellular IL-2 levels and IL-2 receptor expression in activated T cells. These results suggest that suppressive effects of EGCG on T cells is due to both a cell growth arrest and a reduced survival, which might be in turn due to impaired IL-2 signaling as both intracellular IL-2 and expression of its receptor are reduced by EGCG. These findings need to be confirmed in in vivo. Further studies are also needed to determine the molecular mechanism of EGCG-induced cell division arrest. Supported by USDA #58-1950-9-001.