“…The inhibitory effects of triptolide on the maturation and function of DCs have been investigated (Chen et al, 2005;Liu et al, 2007;Zhu et al, 2005). Triptolide prevented the differentiation of DC from monocytes by inhibiting CD1a, CD40, CD80, CD86 and HLA-DR expression, suppressed the LPS-induced maturation of Mo-DCs by blocking CD83 expression and suppressing up-regulation of CD40, CD80, CD86 and HLA-DR, and reduced the capacity of Mo-DC to stimulate lymphocyte proliferation in the allogeneic MLR (Zhu et al, 2005). Another study showed that triptolide treatment not only inhibited the DC maturation and IL-12 production but also decreased the calcium mobilization and chemotactic responses of LPSstimulated DCs to secondary lymphoid tissue chemokine (SLC)/CC chemokine ligand 21 (CCL21) compared to untreated DCs, in association with lower CCR7 and higher CCR5 expression (Chen et al, 2005).…”