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Background  Curcumin is a promising candidate for a natural medicinal agent to treat chronic inflammatory diseases. Although CD4 +  T cells have been implicated in the pathogenesis of chronic inflammation, whether curcumin directly regulates CD4 +  T cells has not been definitively established. Here, we showed curcumin-mediated regulation of CD2/CD3/CD28-initiated CD4 +  T cell activation  in vitro .    Methodology/Principal Findings  Primary human CD4 +  T cells were stimulated with anti-CD2/CD3/CD28 antibody-coated beads as an  in vitro  surrogate system for antigen presenting cell-T cell interaction and treated with curcumin. We found that curcumin suppresses CD2/CD3/CD28-initiated CD4 +  T cell activation by inhibiting cell proliferation, differentiation and cytokine production. On the other hand, curcumin attenuated the spontaneous decline of CD69 expression and indirectly increased expression of CCR7, L-selectin and Transforming growth factor-β1 (TGF-β1) at the late phase of CD2/CD3/CD28-initiated T cell activation. Curcumin-mediated up-regulation of CD69 at late phase was associated with ERK 1/2  signaling. Furthermore, TGF-β1 was involved in curcumin-mediated regulation of T cell activation and late-phase generation of regulatory T cells.    Conclusions/Significance  Curcumin not merely blocks, but regulates CD2/CD3/CD28-initiated CD4 +  T cell activation by augmenting CD69, CCR7, L-selectin and TGF-β1 expression followed by regulatory T cell generation. These results suggest that curcumin could directly reduce T cell-dependent inflammatory stress by modulating CD4 +  T cell activation at multiple levels.

Curcumin Inhibits CD4+ T Cell Activation, but Augments CD69 Expression and TGF-β1-Mediated Generation of Regulatory T Cells at Late Phase