%A Zheng,Long
%A Wang,Xuanchuan
%A Hu,Linkun
%A Gao,Wenjun
%A Zhang,Weitao
%A Zhang,Xuepeng
%A Hu,Chao
%A Rong,Ruiming
%A Yang,Cheng
%A Zhu,Dong
%D 2021
%J Frontiers in Immunology
%C
%F
%G English
%K Cyclic helix B peptide,Antibody-mediated Rejection,Plasma Cells,Germinal Center B cells,Tfh cells,Donor specific antibodies
%Q
%R 10.3389/fimmu.2021.682749
%W
%L
%M
%P
%7
%8 2021-May-12
%9 Original Research
%+ Ruiming Rong,Department of Urology, Zhongshan Hospital, Fudan University,China,rong.ruiming@zs-hospital.sh.cn
%+ Ruiming Rong,Department of Blood Transfusion, Zhongshan Hospital, Fudan University,China,rong.ruiming@zs-hospital.sh.cn
%+ Cheng Yang,Department of Urology, Zhongshan Hospital, Fudan University,China,rong.ruiming@zs-hospital.sh.cn
%+ Cheng Yang,Shanghai Key Laboratory of Organ Transplantation,China,rong.ruiming@zs-hospital.sh.cn
%+ Cheng Yang,Zhangjiang Institute of Fudan University,China,rong.ruiming@zs-hospital.sh.cn
%+ Dong Zhu,Department of Urology, Zhongshan Hospital, Fudan University,China,rong.ruiming@zs-hospital.sh.cn
%+ Dong Zhu,Shanghai Key Laboratory of Organ Transplantation,China,rong.ruiming@zs-hospital.sh.cn
%#
%! CHBP inhibits B cell activation.
%*
%<
%T Cyclic Helix B Peptide Prolongs Skin Allograft Survival via Inhibition of B Cell Immune Responses in a Murine Model
%U https://www.frontiersin.org/articles/10.3389/fimmu.2021.682749
%V 12
%0 JOURNAL ARTICLE
%@ 1664-3224
%X Antibody-mediated rejection (AMR) represents a major cause of allograft dysfunction and results in allograft failure in solid organ transplantation. Cyclic helix B peptide (CHBP) is a novel erythropoietin-derived peptide that ameliorated renal allograft rejection in a renal transplantation model. However, its effect on AMR remains unknown. This study aimed to investigate the effect of CHBP on AMR using a secondary allogeneic skin transplantation model, which was created by transplanting skin from BALB/c mice to C57BL/6 mice with or without CHBP treatment. A secondary syngeneic skin transplantation model, involving transplantation from C57BL/6 mice to C57BL/6 mice, was also created to act as a control. Skin graft rejection, CD19+ B cell infiltration in the skin allograft, the percentages of splenic plasma cells, germinal center (GC) B cells, and Tfh cells, the serum levels of donor specific antibodies (DSAs), and NF-κB signaling in splenocytes were analyzed. Skin allograft survival was significantly prolonged in the CHBP group compared to the allogeneic group. CHBP treatment also significantly reduced the CD19+ B cell infiltration in the skin allograft, decreased the percentages of splenic plasma cells, GC B cells, and Tfh cells, and ameliorated the increase in the serum DSA level. At a molecular level, CHBP downregulated P100, RelB, and P52 in splenocytes. CHBP prolonged skin allograft survival by inhibiting AMR, which may be mediated by inhibition of NF-κB signaling to suppress B cell immune responses, thereby decreasing the DSA level.