Objective: Construction and identification of an chronic antibody-mediated rejection model of renal graft in mice. Methods: Male 6-8 weeks old BALB/cH2d and C57BL/6H2b mice were used as experimental mice and randomly divided into following groups:①The syngeneic control group (SYN14D): no skin transplantation was performed，only C57BL/6H2b to C57BL/6H2b kidney transplantation was conducted，the transplanted kidney was removed 14 days later; ②T cellular-mediated rejection group (TCMR14D): no skin transplantation was performed，only BALB/cH2d to C57BL/6H2b kidney transplantation was conducted，the transplanted kidney was removed 14 days later; ③acute antibody-mediated rejection group (aABMR，BST5D+KT5D): full-thickness back skin transplantation was performed on C57BL/6 mice for 5 days (BALB/CH2d→C57BL/6H2b)，followed by BALB/cH2d to C57BL/6H2b kidney transplantation，the transplanted kidney was removed 5 days later; ④chronic antibody-mediated rejection group 1 (cABMR，TST2D+KT14D): tail skin transplantation was performed on C57BL/6 mice for 2 days(BALB/CH2d→C57BL/6H2b)， followed by BALB/cH2d to C57BL/6H2b kidney transplantation， the transplanted kidney was removed 14 days later; ⑤cABMR group 2 (TST3D+KT14D): tail skin transplantation was performed on C57BL/6 mice for 3 days(BALB/CH2d→C57BL/6H2b)， followed by BALB/cH2d to C57BL/6H2b kidney transplantation， the transplanted kidney was removed 14 days later; ⑥cABMR group 3 (TST4D+KT14D): tail skin transplantation was performed on C57BL/6 mice for 4 days(BALB/CH2d→C57BL/6H2b)， followed by BALB/cH2d to C57BL/6H2b kidney transplantation， the transplanted kidney was removed 14 days later. Pathological staining and Banff score were performed to diagnose the transplanted kidneys，survival curves were plotted，the levels of complement fragment C3d deposition，peripheral blood IgG class donor-specific antibody (DSA)，serum creatinine (Cr) and serum urea nitrogen (BUN) were detected in transplanted kidney tissues，the expression of CD3+T cells，CD19+B cells，F4/80 labelled macrophages，Ly6G labelled myeloid cells was detected. Results: The pathological injury of cABMR group 1 met the diagnostic criteria of ABMR，the postoperative survival rate was 80%，the expression of CD3+T cells was not obvious，so cABMR group 1 was subsequently selected as the model of cABMR for experimental demonstration. Compared with SYN14D，the C3d expression of cABMR was significantly enhanced，the average fluorescence intensity of peripheral blood IgG class DSA was significantly higher，peripheral blood serum Cr and BUN levels were significantly higher. Compared with aABMR，cABMR model of transplanted kidneys showed peritubular capillary haemorrhage and dilatation，single nucleus infiltration seen in the glomeruli，more typical tubular damage and brush border detachment in the tubules， higher Banff scores，significantly more positive areas of C3d expression，significantly higher mean fluorescence intensity of peripheral blood IgG class DSA，significantly higher peripheral blood serum Cr and BUN levels. Compared with aABMR，cABMR group renal interstitial and peritubular capillary CD19+B cells and CD3+T cells infiltration were not significant，renal interstitial F4/80 labelled macrophage and Ly6G labelled myeloid cell infiltration were more significant. Foxp3 and IL-10 expression was significantly reduced in cABMR model， infiltration of IL-1β，IL-6，TNF-α and CCL2 inflammatory cytokines was significantly increased in cABMR model. Conclusion: Our group constructed a cABMR model in which the survival cycle was prolonged，on the basis of which the effects of drug interventions on the prognosis of ABMR patients can be evaluated，which has high clinical application value.