TY - JOUR
T1 - Th2 polarization in target organs is involved in the alleviation of pathological damage mediated by transplanting granulocyte colony-stimulating factor-primed donor T cells
AU - Zhou, Yang
AU - Cao, Leqing
AU - Guo, Huidong
AU - Hong, Yan
AU - Wang, Ming
AU - Wang, Ke
AU - Huang, Xiaojun
AU - Chang, Yingjun
N1 - Publisher Copyright:
© 2020, Science China Press and Springer-Verlag GmbH Germany, part of Springer Nature.
PY - 2021/7
Y1 - 2021/7
N2 - 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) expression 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.
AB - 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) expression 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.
KW - Th2 polarization
KW - graft-versus-host disease
KW - granulocyte colony-stimulating factor
KW - mouse model
UR - https://www.scopus.com/pages/publications/85090158873
U2 - 10.1007/s11427-020-1754-6
DO - 10.1007/s11427-020-1754-6
M3 - Article
C2 - 32880861
AN - SCOPUS:85090158873
SN - 1674-7305
VL - 64
SP - 1087
EP - 1096
JO - Science China Life Sciences
JF - Science China Life Sciences
IS - 7
ER -