FEBS Letters · 2011 · 68 citations · 26 references
Life SciencesMolecular BiologyPharmacologyCell SignalingInnate ImmunitySignal TransductionCell Surface Receptor SignalingCell-surface ReceptorsInflammatory SignalingInnate Immune Signaling PathwaysReceptor-mediated SignalingToll-like ReceptorsCell Surface Toll-like ReceptorsMitogen-activated Protein Kinase CascadesMitogen-activated Protein Kinase PathwaysPro-inflammatory Signaling PathwaysToll-like Receptor AntagonismToll-like Receptor SignalingToll-like Receptor Signaling PathwaysToll-like Receptor-mediated Innate Immune Response
Here we show the molecular basis for the inhibition of peptidoglycan (PGN)-induced TLR2 signaling by a major green tea polyphenol epigallocatechin-3-gallate (EGCG). Recently, we identified the 67-kDa laminin receptor (67LR) as the cell-surface EGCG receptor. Anti-67LR antibody treatment or silencing of 67LR resulted in abrogation of the inhibitory action of EGCG on PGN-induced production of pro-inflammatory mediators and activation of mitogen-activated protein kinases. Silencing of Toll-interacting protein (Tollip), a negative regulator of TLR signaling impaired the TLR2 signaling inhibitory activity of EGCG, suggesting that TLR2 response could be inhibited by EGCG via 67LR and Tollip.
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A receptor for green tea polyphenol EGCG
Hirofumi Tachibana, Kiyoshi Koga, Yoshinori Fujimura et al. · Nature Structural & Molecular Biology · 2004 · 678 citations