Background: Accelerate rejection mediated by CD4+ memory T cells is a key barrior in organt ransplantation, and can hardly be inhibited by current routine immunosupressive agents, such as CsA, FK-506 and rapamycine. In our previously study, we have learned that cpd K, a compond from a famous chinese herbs named Isatis tinctoria L., can pronglong heart survival of re-transplantation recipient and change the proprtion of memory T cells.

Purpose: Here, we want to know whether cpd K could directly inhibit accelarat rejection mediated by CD4+ memory T cells and induce allograft tolerance in a CD4+ memory T cells transfered model, and study the mechnism.

Results: We transferred B6 mice reactive CD4+ memory T cells to naïve B6 mice mice and build a transferred model for this study. And the results demonstrated that cpd K combined with co-stimulatory blockade anti-CD40L and anti-LFA-1 mAbs could effectively inhibit the accelerate rejection mediated by CD4+ memory T cells, and induce allograft tolerance. The treatment could significantly reduce the secretion of IL-2 and IFN-γ, and increase the concentration of TGF-β in the periphery. Of note, a high proportion of regulatory T cells appeared after treatment.

Conclusions: This sudy confirmed that cpd K could inhibit accelerate rejection mediated by CD4+ memory T cells in combination with co-stimulatory blockade, and induce alograft tolerance. This result represent a important step forward in Tm inhibition, whereas detailed mechnism need to be study in the future.