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Green tea EGCG suppresses specific antigen driven T cell response and affects CD4+ T cell differentiation

T cells, in particular CD4+ T helper (Th) cells, play a key role in mediating many aspects of autoimmune diseases. Th1 and the recently discovered Th17 cells are pro‐inflammatory subsets of Th cells, which are responsible for inducing autoimmunity, whereas regulatory T cells (Treg) have a protective effect. Green tea ingredient epigallocatechin‐3‐gallate (EGCG) has been shown to improve symptoms and reduce pathophysiological changes in some animal models of autoimmune diseases. However, the underlying mechanism is not well elucidated, in particular, involvement of Th17 and Treg has not been studied. In this study we found that EGCG inhibited proliferative response of both normal and autoreactive T cells to their specific antigens. This effect was due to its inhibitory effect on both T cells and antigen presenting cells, the former being more significant. EGCG inhibited Th1 but had no effect on Th2 response. Furthermore, EGCG impeded Th1 and Th17 differentiation but promoted Treg development from naïve CD4+ T cells. In the presence of transforming growth factor‐β, interleukin‐6 promoted Th17 and suppressed Treg development, which was diminished by EGCG. Natural Treg population was not affected by EGCG. Together our results indicate that EGCG inhibits Th1 and Th17 differentiation and has no effect on Th2 cells, while it enhances Treg development. These findings help us understand the underlying mechanisms of EGCG‐afforded protection of autoimmune diseases reported in animal models. Future studies are warranted to delineate the impact of EGCG on the regulatory network that controls CD4+ T cell differentiation. Supported by USDA #58‐1950‐7‐707.