%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.