Frontiers in Immunology (Dec 2020)
Inhibition of Glycogen Synthase Kinase 3β Increases the Proportion and Suppressive Function of CD19+CD24hiCD27+ Breg Cells
- Jinyang Li,
- Jinyang Li,
- Jinyang Li,
- Ji Gao,
- Ji Gao,
- Ji Gao,
- Haoming Zhou,
- Haoming Zhou,
- Haoming Zhou,
- Jinren Zhou,
- Jinren Zhou,
- Jinren Zhou,
- Zhenghua Deng,
- Zhenghua Deng,
- Zhenghua Deng,
- Yunjie Lu,
- Yunjie Lu,
- Yunjie Lu,
- Yunjie Lu,
- Jianhua Rao,
- Jianhua Rao,
- Jianhua Rao,
- Guwei Ji,
- Guwei Ji,
- Guwei Ji,
- Jian Gu,
- Jian Gu,
- Jian Gu,
- Xinxiang Yang,
- Xinxiang Yang,
- Xinxiang Yang,
- Yongxiang Xia,
- Yongxiang Xia,
- Yongxiang Xia,
- Xuehao Wang,
- Xuehao Wang,
- Xuehao Wang
Affiliations
- Jinyang Li
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Jinyang Li
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Jinyang Li
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Ji Gao
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Ji Gao
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Ji Gao
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Haoming Zhou
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Haoming Zhou
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Haoming Zhou
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Jinren Zhou
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Jinren Zhou
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Jinren Zhou
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Zhenghua Deng
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Zhenghua Deng
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Zhenghua Deng
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Yunjie Lu
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Yunjie Lu
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Yunjie Lu
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Yunjie Lu
- Hepatopancreatobiliary Surgery, The Third Affiliated Hospital of Soochow University, Changzhou, China
- Jianhua Rao
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Jianhua Rao
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Jianhua Rao
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Guwei Ji
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Guwei Ji
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Guwei Ji
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Jian Gu
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Jian Gu
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Jian Gu
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Xinxiang Yang
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Xinxiang Yang
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Xinxiang Yang
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Yongxiang Xia
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Yongxiang Xia
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Yongxiang Xia
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- Xuehao Wang
- Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Xuehao Wang
- Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, Nanjing, China
- Xuehao Wang
- NHC Key Laboratory of Living Donor Liver Transplantation, National Health Commission, Nanjing, China
- DOI
- https://doi.org/10.3389/fimmu.2020.603288
- Journal volume & issue
-
Vol. 11
Abstract
CD19+CD24hiCD27+ memory Breg cells exhibit decreased abundance in patients with chronic graft-versus-host disease (cGVHD) after liver transplantation and produce less IL-10 than those from patients without cGVHD and healthy donors. Due to the lack of Breg cells and the difficulty in expanding them in vitro, in mouse models and early human clinical trials, the adoptive transfer of Breg cells to autoimmune diseases is greatly restricted. Glycogen synthase kinase 3β (GSK-3β) is a multifunctional serine/threonine (ser/thr) protein kinase that can participate in B cell growth, metabolic activity, and proliferation. Phosphoprotein array analysis showed that p-GSK-3β-s9 was highly expressed in mBreg cells. Furthermore, here, we demonstrated that GSK-3β expression in mBreg cells is lower than that observed in B cells by flow cytometry. We found that the treatment of B cells with the specific GSK-3β inhibitor SB216763 can significantly increase the proportion and immunosuppressive function of mBreg cells in vitro. Nuclear factor of activated T cells (NFAT) is one of a pivotal regulator of gene expression in adaptive immune system. Here, we observed that inhibition of GSK-3β by SB216763 results in enhanced expression of NFATc1 in B cells, which is essential in regulating the ability of B cells to secrete IL-10. By constructing a xGVHD mouse model, we observed that SB216763-treated mBreg cells effectively prevent xenogeneic GVHD. Here we propose a novel strategy using SB216763 to inhibit GSK-3β and then enhance the proportion and immunosuppressive function of mBreg cells by increasing the expression of NFATc1. This approach may be used as a therapy to ameliorate GVHD and inflammatory diseases.
Keywords