【摘 要】
：
Acute graft-versus-host disease(aGVHD)is caused by allo-activated donor T cells infiltrating target organs.As a regulator of immune function,granulocyte colony-stimulating factor(G-CSF)has been demonstrated to relieve the aGVHD reaction.However,the role o
【机 构】
：
Peking University People’s Hospital,Peking University Institute of Hematology,National Clinical Rese
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Acute graft-versus-host disease(aGVHD)is caused by allo-activated donor T cells infiltrating target organs.As a regulator of immune function,granulocyte colony-stimulating factor(G-CSF)has been demonstrated to relieve the aGVHD reaction.However,the role of G-CSF-primed donor T cells in specific target organs is still unknown.In this study,we employed a classical MHC-mismatched transplantation mouse model(C57BL/6 into BALB/c)and found that recipient mice transplanted with G-CSF-primed T cells exhibited prolonged survival compared with that of the PBS-treated group.This protective function against GVHD mediated by G-CSF-primed donor T cells was further confirmed by decreased clinical and pathological scores in this aGVHD mouse model,especially in the lung and gut.Moreover,we found that T cells polarized towards Th2 cells and regulatory T cells were increased in specific target organs.In addition,G-CSF treatment inhibited inducible co-stimulator(ICOS)ex-pression and increased the expression of tolerance-related genes in recipient mice.Our study provides new insight into the immune regulatory effects of G-CSF on T cell-mediated aGVHD,especially for its precise regulation in GVHD target organs.
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