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Green tea EGCG suppresses T cell proliferation by impairing IL‐2/IL‐2R signaling leading to inhibition of cell cycle

Epigallocatechin‐3‐gallate (EGCG), an active ingredient of green tea, has been indicated to have various health benefits. However, little is known about the effect of EGCG on immune function. In this study, we investigated the effect of in vitro EGCG supplementation at physiologically relevant levels on T cell proliferation and its underlying mechanism. Purified T cells were isolated from the spleens of male C57BL/6 mice and stimulated with anti‐CD3/CD28 in the presence of EGCG (2.5‐15 μM). EGCG dose‐dependently inhibited T cell proliferation and cell division, which was more pronounced in CD4+ than in CD8+ T cells. The EGCG‐induced inhibition of T cell division was due to cell cycle arrest as fewer cells entered S‐G2‐M phase. Since IL‐2 is a key factor for T cell proliferation, we determined the effect of EGCG on IL‐2 and IL‐2 receptor (IL‐2R, CD25) levels. Surprisingly, EGCG increased IL‐2 secretion in total T cells. Intracellular staining for IL‐2 indicates that EGCG increased percentage of IL‐2+ cells in CD8+ but not CD4+ population. Furthermore, EGCG reduced the mean intensity of IL‐2 in both CD8+ and CD4+ cells. EGCG did not significantly affect the percentage of CD25+ (IL‐2R) cells but reduced the IL‐2R expression per cell. This suggests that EGCG may inhibit T cell proliferation by inducing cell cycle arrest, which is in turn due to impaired IL‐2/IL‐2R signaling. Increased extracellular IL‐2 might result from decreased internalization and utilization due to less expression of IL‐2R. T cell‐suppressive effect of EGCG might be utilized to ameliorate T cell‐mediated autoimmune diseases.