Epigallocatechin-3-Gallate Directly Suppresses T Cell Proliferation through Impaired IL-2 Utilization and Cell Cycle Progression  

Oleh:

Pae, Munkyong ; Zhihong, Ren ; Meydani, Mohsen

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 140 no. 08 (Aug. 2010), page 1509-1515.
Topik: Cell Cycle Progression; T Cell

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2010.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

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 µmol/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.

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