| First Author | Pae M | Year | 2010 |
| Journal | J Nutr | Volume | 140 |
| Issue | 8 | Pages | 1509-15 |
| PubMed ID | 20534878 | Mgi Jnum | J:162093 |
| Mgi Id | MGI:4462740 | Doi | 10.3945/jn.110.124743 |
| Citation | Pae M, et al. (2010) Epigallocatechin-3-gallate directly suppresses T cell proliferation through impaired IL-2 utilization and cell cycle progression. J Nutr 140(8):1509-15 |
| abstractText | Previously, we demonstrated that in vitro epigallocatechin-3-gallate (EGCG) supplementation inhibited T cell response in mouse spleen cells. In this study, we confirmed this effect of EGCG in mice fed 0.3% EGCG for 6 wk. A coculture with all the combinations of preincubating antigen-presenting cells and T cells with or without EGCG showed that EGCG suppressed antigen-induced T cell proliferation, mainly through a direct effect on T cells. To determine the mechanisms for this effect of EGCG, we stimulated purified mouse T cells with anti-CD3/CD28 in the presence of EGCG (2.5-15 micromol/L) and found that EGCG dose-dependently inhibited cell division and cell cycle progression and this effect of EGCG was more pronounced in CD4(+) than in CD8(+) T cells. Interleukin (IL)-2 concentrations in EGCG-treated cell cultures showed no difference up to 24 h but were higher in the cultures at 48 h compared with the untreated control cells. However, intracellular staining showed no difference between EGCG-treated and untreated control cells in IL-2 synthesis, but EGCG-treated cells expressed less IL-2 receptor (IL-2R) compared with untreated control cells. EGCG did not affect mRNA expression of IL-2 and IL-2R. These results indicate that EGCG-induced IL-2 accumulation in 48 h cultures is due to its reduced utilization. In summary, EGCG directly inhibits T cell proliferative response to both polyclonal and antigen-specific stimulation. CD4(+) cells are more responsive to EGCG than CD8(+) cells. Future studies should determine the effect of EGCG on CD4(+) cell subsets to assess its application in T cell-mediated autoimmune diseases. |
